AntiViral Cancer Research Results
AntiViral, AntiViral: Click to Expand ⟱
Scientific Papers found: Click to Expand⟱
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*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2/PTGS2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE/β-secretase↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.
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*BioAv↑, become increasingly clear in the recent years that 1,8-Cineol spreads almost everywhere in the human body after its oral administration, from the gut to the blood to the brain.
*BBB↑,
*AntiViral↑, anti-viral effects have been observed to include numerous bacteria and fungi species.
*Bacteria↓,
*AntiFungal↑,
*Inflam↓, central mode of action of 1,8-Cineol is the inhibition of pro-inflammatory cytokine expression
*BioAv↑, 1,8-Cineol was detectable in nasal tissue samples after its oral administration for 14 days, which indicates the systemic distribution of 1,8-Cineol via the gut and the blood stream
*MUC2↓, significantly reduced expression levels of the mucin genes MUC2 and MUC19 in close association with a significantly attenuated activity of transcription factor NF-κB
*MUC19↓,
*NF-kB↓, reduced the expression levels of transcriptional activator nuclear factor (NF)-kB p65 and expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in lung tissues
*ICAM-1↓,
*VCAM-1↓,
DNAdam↑, colon cancer cells on the potential genotoxicity of 1,8-Cineol revealed a concentration-dependent increase in oxidative DNA damage, whereas it did not affect the cell viability due to DNA repair mechanisms
*lipid-P↓, suppressing the expression of lipid mediators and prostaglandin D2
*PGE2↓,
*IL4↓, decreased expression levels of different inflammatory cytokines such as interleukin (IL)-4, IL-6 and granulocyte macrophage colony stimulating factor (GM-CSF) in bronchial epithelial cells
*IL6↓,
*IL1β↓, 1,8-Cineol-containing leaf extracts significantly suppressed the expression of pro-inflammatory cytokines IL-1β and IL-6 [
*IL6↓,
eff↑, 1,8-Cineol in combination with ellagic acid has been shown to downregulate different cytokines such as transforming growth factor beta-1 (TGF-β1), Fascin-1 (FSCN1), vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) in p
TGF-β↓,
fascin↓,
VEGF↓,
MMP9↓,
*MAPK↓, 1,8-Cineol was shown to suppress the activation of the MAPK/ERK
*ERK↓,
JNK↓, decreased activities of transcription factor NFκB and the JNK (c-Jun N-terminal kinase)/AP-1 (activator protein-1) pathway in the human cancer cell lines U373 and HeLa in response to 1,8-Cineol, the active ingredient of the drug Soledum
Wnt↓, 1,8-Cineol acts as an inhibitor of the Wnt/β-catenin pathway in head and neck squamous cell carcinoma (HNSCC).
β-catenin/ZEB1↓,
GSK‐3β↑, decreased inhibition of glycogen synthase kinase 3 (GSK-3) and reduced levels of WNT11
*neuroP↑, 1,8-Cineol has been shown to have neuroprotective activity.
*GSK‐3β↓, decreased activity of GSK-3 in response to 1,8-Cineol could ameliorate advanced glycation end products,
*AGEs↓,
*BBB↑, eucalyptol reveals an opening effect on the blood–brain barrier
*NLRP3↓, controls inflammation by suppressing the NOD-like receptor pyrin domain-containing 3 (NLRP3) activation
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NRF2↑, Nanosilver increased Nrf2 protein expression and disrupted the cell cycle at the G1 and G2/M phases.
TumCCA↑, AgNPs interact with DNA to stop
the cell cycle and lead to apoptosis
ROS↑, Nanosilver induced significant mitochondrial oxidative stress in HCT116, whereas it did not in the non-cancer HIEC-6 and nanosilver/sodium ascorbate co-treatment was preferentially lethal to HCT116 cells,
selectivity↑,
*AntiViral↑, AgNPs are effective antiviral agents against various viruses such as human
immunodeficiency virus, hepatitis B virus, and monkey pox virus through interaction with
surface glycoproteins on the virus
*toxicity↝, Citrate and PVP-coated AgNPs have been found to be less toxic than non-coated AgNPs
ETC↓, AgNPs affects mitochondrial function through the disruption of the electron transport
chain2,24,26,33,39–41
MMP↓, Studies have shown that exposure to AgNPs resulted in a decrease of mitochondrial membrane potential (MMP) in various in vitro and in vivo experiments
DNAdam↑, AgNPs has also been shown to interact with and induce damage to DNA, DNA strand breaks, DNA damage
Apoptosis↑, apoptosis induced by AgNPs were through membrane lipid peroxidation, ROS, and oxidative stress
lipid-P↑,
other↝, Several studies have showed AgNPs interact with various proteins such as haemoglobin, serum albumin, metallothioneins, copper transporters, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), malate dehydrogenase (MDH), and bacterial proteins.
UPR↑, Studies have shown exposure to AgNPs induces activation of the UPR
*GRP78/BiP↑, AgNPs induced increased levels of GRP78, phosphorylated PERK, phosphorylated eIF2-α, and
phosphorylated IRE1α, spliced XBP1, cleaved ATF-6, CHOP, JNK and caspase 12
*p‑PERK↑,
*cl‑eIF2α↑,
*CHOP/DDIT3↑,
*JNK↑,
Hif1a↓, One study showed AgNPs inhibits HIF-1 accumulation and suppresses expression of HIF-1 target genes in breast cancer cells (MCF-7) and also found the protein
levels of HIF-1α and HIF-1β decreased
AntiCan↑, Many studies have shown that ascorbic acid, on its own, has anti-cancer effects
*toxicity↓, However, when the rats were treated with both ascorbic acid
and AgNPs, a decrease in toxic effects was observed in non-cancer parotid glands in rats
eff↑, Studies have shown both AgNPs and ascorbic acid have greater effects and toxicity in
cancer cells relative to non-cancer cells
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ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier
Mucositis↓, when compared with iodine alone, the group where iodine and amla gargling were used was very effective in delaying mucositis, reduced incidence of intolerable mucositis
Dose↝, Amla also contains gallic acid, ellagic acid, chebulinic acid, chebulagic acid, emblicanin-A, emblicanin-B, punigluconin, pedunculagin, ellagotannin, trigallayl glucose, chebulagic acid, corilagin and isostrictiniin.
Dose↝, Amla also has a high level of flavonoids like quercetin, kaempferol 3 O alpha L (6″ methyl) rhamnopyranoside and kaempferol 3 O alpha L (6″ ethyl) rhamnopyranoside [4].
*Bacteria↓, Scientific investigations have shown that amla possesses antibacterial, antifungal, and antiviral properties.
*AntiFungal↑,
*AntiViral↑,
*hepatoP↑, Amla also has anti-tussive, anti-atherogenic, hypolipidemic, hepatoprotective, renoprotective, and neuroprotective properties
*RenoP↑,
*neuroP↑,
Dose↝, Briefly, 1% amla mouthwash was prepared by dissolving 1 g of dried amla powder in 100 ml of hot water with vigorous stirring.
*toxicity↓, Chicoric acid is a rare and valuable functional food ingredient with no obvious dose dependence, no overdose side effects, and no contraindications and drug interactions.
*Inflam↓, promising pharmacological effects in regulating glucose and lipid metabolism; anti-inflammatory, antioxidant, and anti-aging properties, and against digestive system diseases
*antiOx↑,
*AntiAge↑,
*eff↝, The amount of chicoric acid is closely related to the plant source, medicinal parts, harvest period, processing, and extraction methods.
*Dose↝, content of chicoric acid in the stems, leaves, and flowers were 9.7%, 44.7%, and 23.6%, respectively
*neuroP↑, neuroprotection effects
*AntiViral↑, its antivirus properties,
*AntiBio↑, Antimicrobial activities for curcumin and rhizome extract of C. longa against different bacteria, viruses, fungi, and parasites have been reported.
*Bacteria↓, These results demonstrated promising antibacterial activity for different curcumin derivatives as well.
*AntiViral↑, Antiviral Activity
*BioAv↓, optimum potential of curcumin is limited because of poor oral bioavailability and insufficient solubility in aqueous solvents leading to poor absorption, fast metabolism, and quick systemic elimination
*Half-Life↓,
*eff↑, Alcoholic extracts from freshly harvested Echinacea purpurea were the strongest, with an 80% reduction of antibiotic treatment days, IRR 0.21 [95% CI 0.15–0.28].
*Imm↑, Echinacea can safely prevent RTIs and associated complications, thereby decreasing the demand for antibiotics.
*AntiViral↑, reported broad-spectrum antiviral effects of alcoholic fresh-plant Echinacea extracts
*antiOx↑, high content of antioxidant and anti-inflammatory substances.
*Inflam↓,
AntiCan↑, anti-cancer effect of EGCG may be related to inhibiting tumour angiogenesis, antioxidant effects and suppressing the inflammatory processes contributing to transformation
Risk↓, Consuming large amounts of EGCG may contribute to reducing the incidence of colorectal cancer, partly due to inhibiting tumour growth factors.
TumCG↓, EGCG is capable of inhibiting growth and inducing apoptosis of cancer cells
Apoptosis↑,
*ROS↓, The main effect of anti-inflammatory and antioxidant substances is to inhibit signalling in the inflammatory process by scavenging ROS
*cardioP↑, EGCG may potentially exert a protective effect on the heart muscle in patients undergoing surgery who are susceptible to ischemic injury,
*Imm↑, The immunomodulatory properties of green tea and its antiviral effect may support the prevention and regulate immune response in infectious diseases, including COVID-19
*AntiViral↑,
*cognitive↑, Consumption of green tea is regarded as an effective dietary intervention to promote clarity of mind and cognitive function.
*antiOx↑, bioactivities of EGCG, including its antioxidant, anti-inflammatory, anticancer, cardiovascular protective, metabolic regulatory, neuroprotective, gut microbiota-modulating, and antimicrobial properties.
*Inflam↓,
*AntiCan↑,
*cardioP↑,
*neuroP↑,
*GutMicro↑,
*AntiBio↑,
*ROS↓, Figure 1, anti inflammatory
*TNF-α↓,
*IL6↓,
TumCP↓,
*LDL↓, cardioprotective
*NO↓,
*Obesity↓, Metabolic syndrome
*p‑tau↓, nervous system
*Aβ↓,
*NRF2↑, , EGCG has been shown to activate the Keap1/P62/Nrf2 signaling pathway,
*SOD↑, upregulation of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, indirectly diminishing the levels of intracellular oxygen free radicals
*Catalase↑,
*GPx↑,
*NLRP3↓, EGCG also restores autophagy levels, suppresses the activation of the NLRP3 inflammasome by inhibiting the mammalian target of rapamycin signaling pathway
*mTOR↓,
TumCCA↑, Cancer: induce cell cycle arrest and inhibit tumor cell proliferation
NRF2↓, EGCG inhibits CCL5-stimulated lung cancer cell proliferation by down-regulating Nrf2 expression
Apoptosis↑, Inducing Apoptosis in Cancer Cells
SIRT1↓, EGCG activates the mitochondrial apoptotic pathway by downregulating SIRT1 expression to modulate the SIRT1-p53 axis
miR-25-5p↓, In breast cancer, EGCG induces apoptosis by inhibiting miR-25 expression and elevating PARP, pre-caspase-3 and pre-caspase-9 protein levels
PARP↑,
Casp3↑,
Casp9↑,
ER Stress↑, in multiple myeloma, EGCG promotes apoptosis by activating the endoplasmic reticulum stress pathway
TumAuto↑, EGCG induces autophagic cell death in breast cancer cells by retaining YAP1 in the cytoplasm and promoting the assembly of the CHMP2B-VPS4B complex
EMT↓, EGCG has been demonstrated to inhibit EMT, invasion, and migration by blocking the TGFβ/Smad signaling pathway
TumCI↓,
TumCMig↓,
TGF-β↓,
Smad1↓,
STAT3↓, EGCG can directly bind to STAT3, reducing nuclear localization and inhibiting the transcription of PLXNC1.
VEGF↓, widely believed that EGCG can block this process by reducing the expression of vascular endothelial growth factor, a key factor in angiogenesis,
angioG↓, The inhibition of angiogenic mimicry by EGCG through the Twist/VE-calmodulin/AKT pathway has also been demonstrated in prostate cancer cells
Imm↑, Acting as an Immunomodulator
EGFR↓, EGCG possesses the ability to interact with EGFR and inhibit activity, strengthening the anticancer evidence for EGCG
*GutMicro↑, EGCG can regulate the balance of gut flora. For example, EGCG can inhibit the growth of harmful bacteria such as Escherichia coli and Salmonella, while promoting the proliferation of probiotics like Bifidobacterium and Lactobacillus
*Bacteria↓, Antibacterial and Antiviral Properties of EGCG
*AntiViral↑,
*BioAv↓, EGCG, its low bioavailability in the human body limits clinical efficacy.
*BioAv↑, Nanotechnology strategy of EGCG.
*eff↑, Co-encapsulation assay of EGCG with quercetin shows that the two synergistically enhanced the antioxidant capacity of EGCG
*BioAv↑, Combining EGCG with resveratrol increases its solubility and significantly improves its absorption in the small intestine.
eff↑, combination of EGCG and curcumin inhibits the activity of metabolic enzymes, reduces the rate of metabolism in the liver and enhances its antitumor efficacy
ChemoSen↑, synergistic effects of EGCG combined with chemotherapeutic agents such as 5-fluorouracil, celecoxib, cisplatin, and tamoxifen have also been reported
*toxicity↝, The European Food Safety Authority notes in scientific opinion that daily oral doses of 800 mg or higher of EGCG represent a common starting point for observed cases of liver injury
AntiCan↑, anticancer, hepatoprotective, antiinflammatory, antioxidant and antimicrobial activities.
*hepatoP↑,
*Inflam↑,
*antiOx↑,
*AntiBio↑,
*BioAv↓, Pharmacokinetic studies have demonstrated that emodin has poor oral bioavailability in rats because of its extensive glucuronidation.
*AntiViral↑, pharmacological effects, such as antiviral, antibacterial, anti‐allergic, anti‐osteoporotic, anti‐diabetic, immunosuppressive, neuroprotective and hepatoprotective activities.
*AntiDiabetic↑,
*neuroP↑,
CSCs↓, Emodin effectively blocked the self‐renewal activity of glioma stem cells by suppressing crucial stemness signalling pathways involving Notch‐1, b‐catenin and STAT3.
NOTCH↓,
β-catenin/ZEB1↓,
STAT3↓,
TumCCA↑, that cells in G2/M phase increased significantly and that the proportion of S‐phase cells gradually declined
*TNF-α↓, inhibiting the serum expression levels of TNF‐α, IL‐6 and IL‐1β
IL6↓,
IL1β↓,
*MMP9↓, emodin treatment effectively inhibited allergen‐induced inflammation by reducing the Th2 immune response, suppressing MMP‐9 expression and inducing HO‐1 expression in a murine model of asthma
*HO-1↑,
cMyc↓, Emodin strongly inhibits the expression of proteins and genes, such as C‐MYC, MCL1, CCND1, CK2, IKK2, PKC, TGF‐β1, Smad4 and Bcl‐2/Bax.
Mcl-1↓,
*diuretic↑, diuretic, vasorelaxant, anti-bacterial, anti-viral, anti-ulcerogenic, anti-inflammatory, and anti-cancer effects.
*Bacteria↓,
*AntiViral↑,
*Inflam↓,
AntiCan↑,
*cardioP↑, timely overview of emodin related to the treatment of cardiovascular disease.
*NF-kB↓, graphic abstract Immunomoduation
*TNF-α↓,
*IL1β↓,
*NO↑,
*eNOS↑,
*PPARγ↑,
*Casp9↓, anti-apoptosis
*Casp3↓,
*GSDMD↓,
*Bcl-2↑,
*STAT3↑,
*ATP↑, anti-oxidant
*SOD↑,
*GSH↑,
*HDAC2↓, anti cardiac hypertrophy
*SIRT3↑,
ROS↑, anti-proliferative
PCNA↓,
P53↑,
cMyc↓,
AntiCan↑, Flavonoids possess a number of medicinal benefits, including anticancer, antioxidant, anti-inflammatory, and antiviral properties.
*antiOx↑,
*Inflam↓,
*AntiViral↑,
*neuroP↑, They also have neuroprotective and cardio-protective effects.
*cardioP↑,
*AChE↓, Apple peel extracts rich in flavonoids inhibits acetylcholinesterase (ACE) in vitro and is an effective antihypertensive agent [17,18,19,20]. It also prevents cardio-metabolic disorders [21] and displays better preservation of cognitive performance w
*cognitive↑,
Risk↓, Flavonoids present in apple are reported to reduce the risk of colorectal cancer. Studies have shown that consumption of one apple per day reduces the chance of cancer up to 50%
*Stroke↓, Stroke Prevention
*AntiDiabetic↑, Antidiabetic Effects
*AntiFungal↑, Antifungal Properties
*ROS↓, Flavonoids have the ability to control the accumulation of reactive oxygen species (ROS) via scavenger ROS when they are formed.
*antiOx↑, these antioxidant compounds have an important role in plant stress tolerance and a high relevance in human health, mainly due to their anti-inflammatory and antimicrobial properties.
*Inflam↓,
*Bacteria↓,
*cardioP↑, anti-inflammatory, anticancer, anti-aging, cardio-protective, neuroprotective, immunomodulatory, antidiabetic, antibacterial, antiparasitic, and antiviral properties
AntiCan↑,
*AntiAge↑,
*AntiDiabetic↑,
AntiViral↑,
*BioAv↓, The bioavailability of flavonoids depends on their class but is, in general, very low. For instance, isoflavones are reported as the most bioavailable flavonoid, more absorbed in the intestine, while other flavonoids, such as galloylated catechins an
*AntiFungal↑, Antifungal Action
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BioAv↝, FMN has only one phenolic hydroxyl group, so it is poorly soluble in water and easily soluble in organic solvents such as methanol, ethyl acetate, and ether.
*memory↑, It had been found that FMN, isolated from Sophora secundiflora, could improve memory problems by restoring the level of oxidative stress in brain tissues and modulating acetylcholinesterase activity. I
*ROS↓, findings suggest that FMN can inhibit oxidative stress in the liver and restore mitochondrial function
*AChE↓,
*NF-kB↓, FMN, the expression levels of the above three decreased and NF-κB activation was inhibited, which may be related to the release of FMN blocking kelch-like ECH-associated protein-1 (Keap1) and activating the nuclear factor erythroid 2-related factor 2
*Keap1↝,
*NRF2↑,
*Inflam↓, FMN exerted anti-neuroinflammatory effects by targeting peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) and bidirectionally regulating NF-κB signaling pathway and Nrf2/Heme oxygenase-1 (HO-1) signaling pathway,
*PGC-1α↝,
*HO-1↓,
*p‑tau↓, thereby inhibiting tau protein hyperphosphorylation.
*cognitive↑, Significantly FMN improve cognitive dysfunction in mice caused by high-fat feeding
*BDNF↑, increased BDNF and 5-hydroxytryptamine (5-HT) levels, and mitigated the progression of depression in mice.
*5HT↑,
*Stroke↓, It could significantly reduce the level of inflammatory factors, increase the number of dendritic spines in neurons, and increase the expression of βIII-tubulin, growth-associated protein 43 (GAP-43), nerve growth factor (NGF) and BDNF.
*PARP1↓, FMN significantly reduced PARP1, PARG, apoptosis-inducing factor (AIF), cysteinyl aspartate-specific protease 3 (caspase-3) and p53 protein in rats with cerebral ischemia-reperfusion injury
*AIF↓,
*Casp3↓,
NP/CIPN↓, FMN had a favorable ameliorative effect on oxaliplatin-induced peripheral neuropathy and did not affect the chemotherapeutic function of oxaliplatin.
*neuroP↑, The neuroprotective mechanism of FMN is shown in Figure 2.
*NGF↑,
*TNF-α↓,
*IL1β↓,
*IL18↓,
*IL6↓,
*VCAM-1↓,
*pol-M2 MC↑,
*hepatoP↑, could reduce hepatotoxicity and improve liver function through inflammatory molecular pathways.
*AST↓, reduce serum AST, ALT, TNF-α and IL-1β levels. I
*ALAT↓,
*LC3II↑, the levels of LC3II, Beclin1, p62, cyclooxygenase-2 (COX2), COX4, MMP and adenosine triphosphate (ATP) were increased
*Beclin-1/ATG6↑,
*p62↑,
*COX2/PTGS2↑,
*MMP↑,
*ATP↑,
*GSH↑, activity of antioxidant proteins glutathione (GSH), catalase (CAT), GSH-PX in the FMN treatment group recovered, and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) decreased.
*Catalase↑,
*GPx↑,
*MDA↓,
*antiPs↑, it was found that the interferon (IFN) signaling pathway was inhibited, which could effectively reduce the expression of related inflammatory chemokines, and significantly improve the erythema, scales and thickness of skin lesions in the psoriasis m
*AntiDiabetic↑, FMN effectively mitigated alloxan-induced pancreatic β-cell and DNA damage, lowered blood glucose levels, and increased insulin content.
*glucose↓,
*Insulin↑,
*GutMicro↑, FMN could act as a prebiotic to regulate intestinal microbial flora, thereby improving host metabolism and preventing obesity
*Obesity↓,
COX2/PTGS2↓, FMN effectively inhibited the proliferation of KYSE170 and KYSE150 cells by significantly reducing the mRNA and protein expression levels of COX-2 and cyclin D1, while inducing G1 phase arrest.
cycD1/CCND1↓,
TumCCA↑,
EGFR↓, FMN binds to both WT and mutant EGFR, reducing EGFR kinase activity and inhibiting downstream signaling.
GSK‐3β↑, This, in turn, activated GSK-3β and decreased the expression of myeloid leukemia sequence 1 (Mcl-1), without causing significant toxicity to the vital organs of mice.
Mcl-1↓,
*toxicity↓,
TumCP↓, FMN inhibited the proliferation and growth of cervical cancer cells by inhibiting the expression of HIF-1-α and VEGF.
Hif1a↓,
VEGF↓,
ERK↓, can achieve antiproliferative and invasive effects through effective inhibition of the oncogenic ERK1/2 pathway and the Lamin A/C signaling pathway,
LAMs↓,
Cyt‑c↑, FMN, as a candidate anticancer drug, could release cytochrome C (cyto C) directly through the mitochondrial pathway and activate the cascade reaction of caspase-9, caspase-3 and PARP, which ultimately lead to FaDu cell death
Casp9↑,
Casp3↑,
PARP↑,
TumCD↑,
mitA↑, FMN inhibited mitosis by inactivating the BACH1/p53 signaling pathway, promoted the release of cyto C
BACH1↓,
P53↓,
ROS↑, FMN delivered ROS to mitochondria to release cyto C and activated caspase-3 and caspase-9 cascade reactions to induce apoptosis in MCF7 cells
PD-1↓, FMN has the potential to serve as a PD-1/PD-L1 inhibitor for clinical use
NF-kB↓, FMN mainly interfered with PD-L1 activation by inhibiting the STING-NF-κB signaling pathway
*Bacteria↓, possess other pharmacological activities, such as antibacterial, antiviral, and antiallergic
*AntiViral↑,
*mt-ROS?, FMN effectively reduced the accumulation of ROS and mitochondrial damage in hair cells by activating the PI3K/AKT-Nrf2 signaling pathway, restored the balance of GSH/GSSG.
*PI3K↓,
*chemoP↑, FMN was a potential therapeutic agent for cisplatin-induced ototoxicity.
ChemoSen↑, Therefore, combination therapy had better control effects on multiple targets and a lower risk of drug resistance, which had great application prospects for treating cancer.
eff↑, combination of FMN (30 μM) and sulforaphane (20 μM) exhibited a significant synergistic effect
*toxicity↓, Therefore, it was proved that FMN was safe and non-toxic and could be used for pharmacological and therapeutic purposes.
*BioAv↑, water solubility problem of FMN, succinylated FMN using Bacillus amyloliquefaciens FJ18 to form the compound FMN-7-O-β-D (6″-O-succinyl)-D-glucoside (FMP), which compared to FMN, the water solubility was increased more than 106-fold.
*BioAv↑, To solve those problems, structural modification and nano-delivery systems can be used as a promising solution
*eff↑, FMN can be combined with other treatments, such as immunotherapy, to enhance the therapeutic effect and improve the prognosis of patients;
*Dose↝, 0, 3, 6, and 9 h after ingestion of 3 g of fucoidan.
*BioAv↝, 332.3 ± 357.6 μg/gCr in subjects living in Okinawa prefecture, compared with 240.1 ± 302.4 μg/gCr in subjects living outside Okinawa
*eff↝, Okinawa prefecture than in those living outside Okinawa prefecture, the habit of eating mozuku was speculated to be a factor in the absorption of fucoidan
*Inflam↓, Fucodan exhibits many different biological properties, including anti-inflammatory, anticoagulant, antithrombotic, antiadhesive, antiangiogenic, antiviral, antitumor and antioxidant activities
*AntiThr↑,
angioG↓,
*AntiViral↑,
*AntiTum↑,
*antiOx↓,
*BioAv↝, The rate of absorption through the small intestine was highly variable among the participants.
*toxicity↓, Fucoidan is a versatile, nontoxic marine-origin heteropolysaccharide that has received much attention due to its beneficial biological properties and safety.
*AntiViral↑, ucoidan has been demonstrated to exhibit a variety of conventional bioactivities, such as antiviral, antioxidant, and immune-modulatory characteristics, and anticancer activity against a wide range of malignancies has also recently been discovered.
*antiOx↑,
*Imm⇅,
AntiCan↑,
TumCCA↑, Fucoidan inhibits tumorigenesis by prompting cell cycle arrest and apoptosis, blocking metastasis and angiogenesis, and modulating physiological signaling molecules.
Apoptosis↑,
TumMeta↓,
angioG↓,
antiNeop↑, Fucoidans’ capacity to bind to Toll-like receptors and intervene with the action of vascular endothelial growth factors (VEGF) and matrix metalloproteinases (MMPs) could explain their anti-neoplastic properties
VEGF↓,
MMPs↓,
BioAv↑, Low molecular weight fractions (LMWF), in particular, are thought to be more biocompatible [47]
BioAv↑, in rats, following topical administration of fucoidan (MW 750 kDa) from Fucus vesiculosus demonstrated fine skin-penetrating characteristics.
ROS⇅, Induction/inhibition of reactive oxygen species (ROS), mitochondrial instability, and caspase and poly (ADP-ribose) polymerase (PARP) cleavage are all aspects of it
cl‑PARP↑, fucoidan treatment causes PARP cleavage and caspase-3/7 activation in MCF-7 cells, which are hallmarks of apoptosis [
Casp3↑,
Casp7↑,
ROS↑, human hepatoma SMMC-7721 cells, fucoidan therapy caused noteworthy growth inhibition and ROS-mediated apoptosi
GSH↓, lower glutathione consumption (GSH), mitochondrial swelling, and depolarization of the mitochondrial membrane potential
MMP↓,
PI3K↓, Fucoidan inhibits PI3K, suppressing ERK and activates MAPK, limiting cancer cell proliferation and decreasing Bcl-2 to Bax ratio, inducing caspase-dependent apoptosis in BEL-7402 and LM3 cell lines
ERK↓,
MAPK↑,
TumCP↓,
Bax:Bcl2↑,
TJ↑, Meanwhile, dietary fucoidan progressively restores intestinal villi by upregulating the expression of tight junction proteins such as ZO-1, Occludin, Claudin-1, and Claudin-8 via p38 MAPK and ERK1/2 activation.
ZO-1↑,
OCLN↑,
CLDN1↑,
IBI↑, fucoidan supplementation improves intestinal barrier function by enhancing intestinal microbiota diversity
GutMicro↑,
NK cell↑, ↑NK cell-mediated anticancer immunity
STAT3↓, Inhibits STAT3 Signaling
eff↑, Astragalus polysaccharide as a topical mucosal adjuvant to boost the anticancer efficacy of immune checkpoint inhibitors
TumCCA↑, Among the anticancer mechanisms of fucoidan are cell cycle arrest, apoptosis evocation, and stimulation of cytotoxic natural killer cells and macrophages.
Apoptosis↑,
NK cell↑,
chemoP↑, Fucoidan also protects against toxicity associated with chemotherapeutic drugs and radiation-induced damage.
TumCG↓, fucoidan slows tumor growth, kills cancer cells, and interacts with cancer chemotherapy drugs.
*Inflam↓, fucoidan has countless superior biological activities, which include anti-inflammatory, antioxidant, anticlotting, antithrombotic, antiviral, anti-angiogenesis, and anti-Helicobacter pylori activities
*antiOx↑,
*AntiThr↑,
*AntiViral↑,
angioG↓,
ChemoSen↑, Furthermore, LMWF complexed with tamoxifen, cisplatin, or paclitaxel shows cell growth inhibition, cellular apoptosis, and arrest of the cell cycle in the human breast cancer cell line MCF-7/ MDA-MB-231.
ROS↑, The study revealed that in breast cancer cells, phosphorylation of different proteins, elevation the reactive oxygen species (ROS) levels, and reduced glutathione (GSH) levels were all crucial in cancer cell apoptosis
GSH↓,
mtDam↓, reatment with fucoidan leads to increased levels of ROS in cells, along with mitochondrial damage and mitochondrial membrane potential (MMP) depolarization.
MMP↓,
DNMT3B↓, inhibition of its downstream target DNA methyltransferase 3B (DNMT3B) by the administration of a fixed dose of fucoidan
TumCG↓, Oral administration of fucoidan (5 mg/kg) effectively inhibited tumor growth in mice grown with B16 melanoma cells.
Dose↝, fucoidan (5 mg/kg) effectively inhibited tumor growth in mice
Dose↝, Twenty patients with advanced cancer were selected for the study, in which oral fucoidan (4 g daily) was administered for at least four weeks. After two consecutive weeks of ingestion, there was a significant reduction in the levels of key proinflamm
QoL∅, but no significant change was observed in patients’ quality of life, including the experience of fatigue
fatigue∅,
Dose↝, 300 mg fucoidan is safe and well tolerated by humans
antiOx↑, anti-oxidant, antiviral, immunoregulatory, anti-coagulant, anti-thrombotic, anti-lipidemic, anti-diabetic, anti-tumor, anti-metastatic, and anti-angiogenic properties
AntiViral↑,
Imm↝,
*AntiThr↑,
*AntiDiabetic↑,
AntiTum↑,
TumMeta↑,
angioG↓,
Hif1a↓, ↓ HIF-1α and VEGF in hypoxic-like conditions
VEGF↓,
MMPs↓, ↓ MMPs
EMT↓, ↓ EMT (↓ N-cadherin; ↑ E-cadherin)
N-cadherin↓,
E-cadherin↑,
TIMP1↑, ↑ TIMP
PI3K↓, ↓ PI3K/Akt/mTOR
Akt↓,
mTOR↓,
MMP2↓, ↓ MMP-2, 9
ChemoSen↑, available findings indicate that oral intake of fucoidan as dietary supplement in combination with conventional adjuvant chemotherapy can prolong survival time, decrease some adverse effects (e.g., fatigue)
OS↑,
fatigue↓,
CD31/PECAM-1↓, fig 2
angioG↓, anti-angiogenesis, anti-metastasis, synergistic effects and chemo-sensitization.
TumMeta↓,
ChemoSen↑, GA was reported to increase the intracellular concentration at lower doses of chemotherapeutic drug that helped develop it for combinatorial therapy to exploit its synergistic activity to selectively target cancer cells.
*cardioP↑, biological activities including anticancer, anti- cardiovascular disease (CVD) antiinflammatory, anti-viral, anti-parasitic, anti-infectiousness, antioxidant, and a promising molecule to treat osteoarthritis
*Inflam↓,
*AntiViral↑,
*antiOx↑,
NF-kB↓, suppressing NF-κB activity through modification of 179Cys of IKKβ moieties, resulting decreased expression of TNFα, COX-2, and iNOS
TNF-α↓,
COX2/PTGS2↓,
iNOS↓,
Apoptosis↑, apoptosis, autophagy and suppressing propagation and invasion of cancer cells
TumAuto↑,
TumCP↓,
TumCI↓,
BioAv↓, clinical applications are severely limited due to the poor aqueous solubility (0.013mg/mL) requiring repeat injections.
ROS↑, GA enhances production of reactive oxygen species (ROS) by collapsing the mitochondrial transmembrane potential (MMP), increasing downregulation of SIRT1 in multiple myeloma
MMP↓,
SIRT1↓,
Akt↓, GA inhibits AKT/mTOR complex 1 (mTORC1) by upregulating (AMP-activated protein kinase) AMPK and LRIG1 (leucine-rich repeats and immunoglobulinlike domains 1)
mTORC1↓,
AMPK↑,
LRIG1↑,
ER Stress↑, The inhibition of proteasomal system by GA contributes to the dilation of ER and induces ER stress and mitochondrial membrane depolarization leading to the formation of mega-mitochondria in treated cancer cells.
Paraptosis↑, GA induces paraptosis in cancer cells
Ferroptosis↑, GA induced ferroptosis in HCT116 colon cancer cells was observed
HSP90↓, GA directly inhibits the expression of HSP90, a pleiotropic regulator of multiple signalling pathways, and increases the GSH depletion leading to an increased level of LPOs and ultimately the cell undergoes ferroptosis.
GSH↓,
lipid-P↑,
GPx4↓, figure 4
miR-21↓, GA regimens also decreased the miR-21 expression and blocked PI3K/Akt signaling pathway by enhancing PTEN activity [48].
PI3K↓,
Akt↓,
PTEN↑,
ASAP2↓, GA inhibited the proliferation, migration and invasion by downregulating the expression of ASAP2 and CDK7
CDK7↓,
AntiTum↑, As inhibitors of SUMOylation, GAs demonstrate significant antitumor activity, and can exert antineoplastic effects through multiple pathways, which positions them as potentially promising therapeutic agents for cancer treatment.
SUMO↓,
antiNeop↑,
*Inflam↓, GAs exhibit notable anti-inflammatory, antibacterial, and antiviral properties, highlighting their multifaceted medicinal potential.
*Bacteria↓,
*AntiViral↑,
*toxicity↑, the associated risks of liver and kidney damage must not be overlooked. GAs can induce significant hepatic damage by promoting cellular apoptosis, oxidative stress, and the disruption of various metabolic processes.
*ROS↑,
*toxicity↝, Due to their recognized toxicity, the concentration of GAs is typically regulated to within 5ppm in the standardized G. biloba leaf extract EGb 761.
*Inflam↓, G. biloba exerts its effects through its anti-inflammatory, anti-apoptotic, anti-cancer, neuroprotective, cardioprotective, hepatoprotective, antiviral, antibacterial, pulmoprotective, renoprotective, anti-osteoporosis, anti-melanogenic, ...
*Apoptosis↓,
*neuroP↑,
*cardioP↑,
*hepatoP↑,
*AntiViral↑,
*Bacteria↓,
*RenoP↑,
*ROS↓, The most important mechanisms involved in these actions are altering the elevation of ROS formation, inhibiting NADPH oxidases activation
*NADPH↓,
*MAPK↓, downregulating MAPKs (p38 MAPK and ERK, and JNK) and AP-1, increasing cAMP, inactivating Stat5,
*ERK↓,
*JNK↓,
*AP-1↓,
*cAMP↑,
*STAT5↓,
*AMPK↑, activating the AMPK signaling pathway
AntiTum↑, Germanium has long been considered a therapeutic agent with anticancer, antitumor, antiaging, antiviral and anti-inflammatory effects.
AntiCan↑,
*AntiAge↑,
*AntiViral↑,
*Inflam↓,
*NK cell↑, Bio-Germanium group exhibited NK cell activity increases at effector cell:target cell (E:T) ratios of 50:1, 10:1, 5:1 and 2.5:1
*Imm↑, confirm that Bio-Germanium acts as an effective immunostimulant by increasing the cytotoxicity of NK cells and activating immunoglobulin, B cells and tumor necrosis factor (TNF)-α (P<0.05).
*TNF-α↑,
TumCP↓, genistein inhibits cervical cancer cell proliferation and induces apoptosis
Apoptosis↑,
RadioS↑, Use of genistein in combination with radiation or chemotherapy agents resulted in enhanced response indicating radio- and chemo-sensitization properties.
ChemoSen↑,
*antiOx↑, evidence that genistein has antioxidant [17], anti-inflammatory [18], antibacterial [19], antiviral [20,21], antidiabetic [22,23], neuroprotective [24,25], and anti-cancer [26,27,28] effects.
*Inflam↓,
*Bacteria↓,
*AntiViral↑,
*AntiDiabetic↑,
*neuroP↑,
AntiCan↑,
TumCG↓, genistein had reduced cell growth and invasion, and increased cell cycle arrest and apoptosis
TumCI↓,
TumCCA↑,
cl‑PARP↑, increased levels of cleaved poly (ADP-ribose) polymerase (PARP), a marker of apoptosis, after treatment with genistein in HeLa cells,
selectivity↑, while no cleaved PARP was seen in L929 cells (normal mouse fibroblasts).
CycB/CCNB1↓, decreased protein expression of cyclin B1 and cyclin-dependent kinase 1 (CDK1), and decreased tyrosine phosphorylation of cell division control protein 2 (cdc2)
CDK1↓,
p‑cDC2↓,
p‑ERK↓, genistein inhibits cell growth and decreases cell viability through decreasing the phosphorylation/activation of ERK, while increasing phosphorylation/activation of p38 and JNK
p‑p38↑,
p‑JNK↑,
MMP9↓, decrease in mRNA expression of MMP-9 and an increase in TIMP-1 expression
TIMP1↑,
BioAv↓, Genistein has low solubility and bioavailability.
BioAv↑, Nanoparticle technology has been employed for the encapsulation and delivery of compounds with low absorption and bioavailability.
Half-Life↑, Despite its low bioavailability, genistein has a long half-life of 46 h in vivo
*antiOx↑, reported in preclinical studies, such as the antioxidant, anti-inflammatory, antibacterial, and antiviral activities
*Inflam↓,
*Bacteria↓,
*AntiViral↑,
*Dose↝, the most genistein-rich foods are those fermented (miso and natto), which contain 38.5-230 μg/g of genistein, due to the β-glycosyl bond cleavage of genistin (7-O-β-D-glucoside form of genistein, naturally occurring in plants) by microbes during the
*AntiDiabetic↑, figure 1
angioG↑, In the low concentration (0.001–1 μM), genistein induced angiogenesis by promoted tube formation.
Apoptosis↑, Neuroblastoma IMR-32 SK-N-BE2 ↑Apoptosis, ↓cell viability, ↑Myd88, ↑Beclin 1, ↑LC3 II, ↑TLR4, ↑autophagy, ↓mTOR, ↓p62
tumCV↓,
MyD88↑,
Beclin-1/ATG6↑,
LC3II↑,
TLR4↑,
TumAuto↑,
mTOR↓,
p62↓,
TumCCA↑, SK-N-SH ↑Cell cycle arrest at phase G2/M, ↓proliferation, ↑Akt, ↑CHD5, ↑p53, ↓neuroblastoma growth, ↓tumor microvessel formation, ↓DNMT3b, ↑ERE, ↑luciferase, ↑MEK
TumCP↓,
Akt↑,
P53↑,
DNMT3B↓,
MEK↓,
hTERT/TERT↓, ↓hTERT, ↓VEGF, ↓NF-κB, ↓c-IAP2, ↓MDR, ↓N-Myc, ↓FGF2, ↓p-Ak
VEGF↓,
NF-kB↓,
IAP1↓,
MDR1↓,
p‑Akt↓,
eff↑, There is synergistic efficiency of genistein and sorafenib (SF) combined treatment in human malignant neuroblastoma SH-SY5Y (
ChemoSen↑, Genistein has no special effect on P-gp function, but it boosts up the intracellular accumulation of doxorubicin
AntiCan↑, A.muricata’s activities were shown to include anticancer (25%), antiulcer (17%), antidiabetic (14%), antiprotozoal (10%), antidiarrhea (8%), antibacterial (8%), antiviral (8%), antihypertensive (6%), and wound healing (4%).
*AntiDiabetic↑,
*Diar↓,
*Bacteria↓,
*AntiViral↑,
*Wound Healing↑,
MMP2↓, Fruit, stem, seed, and twigs Inhibits MMP-2 and MMP-9, which play an important role in cancer progression, in HT1080 fibrosarcoma cells.
MMP9↓,
MMP↓, Disrupts MMP function, reactive oxygen species (ROS) generation, and G0/G1 cell cycle arrest in HL-60 leukemia cells.
ROS↑,
TumCCA↑,
BAX↑, Increases Bax expression and decreases Bcl-2 expression, cell cycle arrest at G0/G1 phase in A-549 lung cancer cells.
Bcl-2↓,
Casp3↑, Induces apoptosis by enhancing the expression of caspase-3 in MDA-MB-231 breast cancer cells.
*BAX↓, Antiulcer Leaf, Downregulates Bax and malondialdehyde (MDA) expression.Upregulates CAT, SOD, GSH, NO, PGE2, glycogen, and Hsp70 expression.
*MDA↓,
*Catalase↑,
*SOD↑,
*GSH↑,
*NO↑,
*PGE2↑,
*HSP70/HSPA5↑,
*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection
| - |
in-vitro, |
Melanoma, |
SK-MEL-28 |
|
|
|
*Inflam↓, Isoliquiritigenin (ISL), a phenolic compound derived from licorice, exhibits various biological activities, including anti-inflammatory, anti-viral, anti-tumor, and antioxidant effects
*AntiViral↑,
*AntiTum↑,
*antiOx↑,
cl‑Casp9↑, ISL treatment induces apoptosis in SK-MEL-28 cells, as evidenced by the cleavage of caspase-9, -7, -3, and PARP.
cl‑Casp7↑,
cl‑Casp3↑,
cl‑PARP↑,
BAX↑, ISL increased Bax expression, decreased Bcl-2 expression, and promoted cytochrome C release into the cytosol.
Bcl-2↓,
Cyt‑c↑,
cycD1/CCND1↓, ISL also reduced the expression of cell cycle markers, including cyclin D1, D3, and survivin.
cycD1/CCND1↓,
survivin↓,
ROS↓, Notably, ISL treatment markedly increased intracellular ROS levels
eff↓, pretreatment with N-acetyl cysteine(NAC), a ROS scavenger, abrogated the ISL-induced inhibition of the p38/mTOR/STAT3 pathway and prevented apoptosis.
p‑mTOR↓, ISL significantly diminished the constitutive phosphorylation of mTOR and STAT3 in SK-MEL-28 cells by blocking the phosphorylation of p38 MAPK
p‑STAT3↓,
p‑MAPK↓,
JAK↓, ISL exerts significant anti-ovarian cancer effects through multitarget regulation of the JAK/STAT pathway.
STAT↓,
toxicity↓, With the advantages of low toxicity and multi-pathway modulation, ISL is a promising natural candidate for targeted therapy,
*antiOx↑, exhibits significant antioxidant capacity, effectively scavenging free radicals and reducing oxidative stress-induced cellular damage
*ROS↓,
*NRF2↑, By activating the Nrf2/ARE signaling pathway, ISL induces the expression of antioxidant enzymes such as HO-1 and NQO1, thereby enhancing cellular antioxidant defense systems
*ARE↑,
*HO-1↑,
*NQO1↑,
*Inflam↓, Regarding anti-inflammatory effects, ISL suppresses NF-κB and MAPK signaling pathways, reducing inflammatory factor production and alleviating inflammatory responses
*NF-kB↓,
*MAPK↓,
*SOD↑, it maintains intracellular antioxidant defense mechanisms, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activity to mitigate oxidative stress-induced cellular damage
*Catalase↑,
*GPx↑,
*AntiViral↑, Its antiviral activity manifests as ISL’s ability to disrupt viral replication cycles, inhibit viral protein synthesis, and suppress multiple viruses.
*NADPH↑, ISL reduces ROS production by activating the Nrf2 pathway or upregulating NADPH oxidase expression and activity
ROS↓, In SK-MEL-28 melanoma cells, ROS inhibition suppressed p38α (Thr180/Tyr182) phosphorylation, blocked the p38-mTOR-STAT3 (Ser727) cascade. This leads to decreased STAT3 transcriptional activity, silencing downstream cyclin D1 and survivin expression,
p38↓,
mTOR↓,
STAT3↓,
cycD1/CCND1↓,
survivin↓,
p38↑, ISL inhibits autophagy flux in pancreatic cancer cells by activating the p38-MAPK signaling pathway,
MAPK↑,
mtDam↑, This mechanism disrupts cellular clearance of damaged mitochondria, triggers endoplasmic reticulum stress and oxidative stress, ultimately inducing apoptosis.
ER Stress↑,
ROS↑,
Apoptosis↑,
GLUT4↓, chemically synthesized derivative ISL-17 in MKN45 gastric cancer cells interferes with energy metabolism (Warburg effect) by inhibiting GLUT4-mediated glucose uptake, leading to decreased ATP levels and increased ROS accumulation.
ATP↓,
Glycolysis↓, This process triggers an energy crisis by blocking glycolysis and oxidative phosphorylation, further enhancing the cytotoxic effects of ROS and thereby inhibiting tumor growth
eff↑, Combining ISL with mTOR inhibitors significantly enhances growth inhibition of ovarian cancer cells by dual blockade of the PI3K/Akt/mTOR pathway
| - |
NA, |
neuroblastoma, |
SH-SY5Y |
|
|
|
*toxicity↑, Ivermectin (IVM) could cause potential neurotoxicity; however, the precise molecular mechanisms remain unclear.
TumCD↑, The results show that IVM treatment (2.5–15 μM) for 24 h could induce dose-dependent cell death in SH-SY5Y cells.
ROS↑, Compared to the control, IVM treatment significantly promoted the production of ROS, mitochondrial dysfunction, and cell apoptosis.
mtDam↑,
Apoptosis↑,
MitoP↑, IVM treatment also promoted mitophagy and autophagy, which were charactered by the decreased expression of phosphorylation (p)-Akt and p-mTOR proteins, increased expression of LC3II, Beclin1, ATG5, PINK, and Pakin1 proteins and autophagosome formatio
TumAuto↑,
p‑Akt↓,
p‑mTOR↓,
LC3II↑,
Beclin-1/ATG6↑,
ATG5↑,
PINK1↑,
PARK2↑,
tumCV↓, At 6 h and 12 h, IVM treatment at 15 μM significantly decreased the cell viabilities to 44.3% and 35.6% (both p < 0.01), respectively;
MDA↑, IVM treatment at the doses of 10 and 15 μM significantly increased the levels of MDA to 0.25 nmol/mg and 0.76 nmol/mg protein (both p < 0.01) (Figure 3B), respectively; increased the activities of SOD to 1.61 U/mg and 3.48 U/mg protein (both p < 0.
SOD↑,
Catalase↑,
eff↓, NAC treatment at 10 mM significantly inhibited the IVM-induced production of ROS
MMP↓, IVM treatment significantly decreased the ΔΨm in a dose-dependent manner.
BAX↑, IVM treatment significantly increased the expressions of Bax, cleaved caspase-3, cleaved caspase-9, cleaved PARP-1 proteins, and CytC proteins, and decreased the expressions of Bcl-2 and pro-caspase-3 proteins.
cl‑Casp3↑,
cl‑Casp9↑,
cl‑PARP↑,
Cyt‑c↑,
Bcl-2↓,
proCasp3↓,
Bax:Bcl2↑, IVM treatment at 10 μM significantly increased the ratio of Bax/Bcl-2 to 2.6-fold
eff↑, Inhibition of Autophagy Improves Ivermectin-Induced Cytotoxicity, Oxidative Stress, and Apoptotic Cell Death
*AntiP↑, IVM has been widely used as an antiparasitic drug in human and veterinary medicines
*Inflam↓, IVM exhibited several new threptic effects, including anti-cancer, anti-inflammation, anti-diabetic, and antiviral effects
*AntiDiabetic↑,
*AntiViral↑,
BBB∅, In relation to the current recommended dose, IVM is not thought to readily cross the blood–brain barrier in humans
toxicity↝, It has been reported that an IVM overdose could induce neurotoxicity in SARS-CoV-2 patients and the main neurotoxic symptoms include confusion, ataxia, weakness, hypotension, and seizures
| - |
in-vitro, |
CRC, |
SW480 |
|
|
|
- |
in-vivo, |
CRC, |
HCT116 |
|
|
|
*AntiP↓, Ivermectin, an antiparasitic drug, has been shown to possess anti-inflammation, anti-virus, and antitumor properties.
*Inflam↓,
*AntiViral↑,
AntiTum↑,
TumCP↓, ivermectin dose-dependently inhibited colorectal cancer SW480 and SW1116 cell growth, followed by promoting cell apoptosis and increasing Caspase-3/7 activity.
Apoptosis↑,
Casp3↑,
Casp7↑,
BAX↑, ivermectin upregulated the expression of proapoptotic proteins Bax and cleaved PARP and downregulated antiapoptotic protein Bcl-2.
cl‑PARP↑,
Bcl-2↓,
mt-ROS↑, ivermectin promoted both total and mitochondrial ROS production in a dose-dependent manner,
eff↓, which could be eliminated by administering N-acetyl-l-cysteine (NAC) in CRC cells.
Dose↝, ivermectin at low doses (2.5 and 5 µM) induced CRC cell arrest. Overall, ivermectin suppressed cell proliferation by promoting ROS-mediated mitochondrial apoptosis pathway and inducing S phase arrest in CRC cells,
TumCCA↑,
*importin α/β↓, ivermectin targets the ability of importin-α (Imp-α) to recognize nuclear localization sequences, without effecting the Imp-α/β1 interaction.
*AntiViral↑, ivermectin inhibits genome replication of HAdV-B3, a clinically important pathogen responsible for numerous recent outbreaks
*Inflam↓, Juglone is an anthraquinone with anti-inflammatory, antiviral, and anti-cancer properties that have shown promise in inhibiting tumor cell growth.
*AntiViral↑,
*AntiCan↑,
ROS↑, promoting intracellular ROS generation and upregulating the expression level of p53 protein, thereby inhibiting the progression of colorectal cancer
P53↑,
TumCP↓,
*neuroP↑, Studies have reported the neuroprotective effects of Lico-A, suggesting its potential as a multitarget compound.
*PTP1B↓, Lico-A acts as a PTP1B inhibitor, enhancing cognitive activity through the BDNF-TrkB pathway and exhibiting inhibitory effects on microglia activation, which enables mitigation of neuroinflammation
*cognitive↑,
*BDNF↑,
*TrkB↝, It not only enhances cognitive activity via the BDNF-TrkB pathway
*cJun↓, Moreover, Lico-A inhibits c-Jun N-terminal kinase 1, a key enzyme involved in tau phosphorylation,
*p‑tau↓,
*AChE↓, Lico-A also acts as an acetylcholinesterase inhibitor, leading to increased levels of the neurotransmitter acetylcholine (Ach) in the brain.
*Ach↑,
*Aβ↓, Lico-A has shown the ability to reduce amyloid plaques, a hallmark of AD, and exhibits antioxidant properties by activating the nuclear factor erythroid 2-related factor 2 (Nrf2)
*antiOx↑,
*NRF2↑,
*AntiViral↑, figure 1
*Obesity↓,
*PI3K↑, The proposed mechanism is through the activation of the PI3K/Akt/mTOR
*Akt↑,
*mTOR↑,
*memory↑, Licochalcone A as an Acetylcholinesterase Inhibitor and Memory Enhancer
*BBB↑, Furthermore, its ability to penetrate the blood–brain barrier (BBB)
Dose↝, Test group (15 patients) received oral bLF 250 mg/day beside chemotherapy for three months. Control group (15 patients) received chemotherapy only.
toxicity↓, 3 months after treatment indicates that no significant difference in mean values of serum creatinine, AST, ALT, serum LF, serum GST enzyme, INF-γ, WBCs count, platelet count, CEA, RBCs count, neutrophil count, and Hb level of patients
INF-γ↝, Mean percent of change of main parameters (serum LF, serum GST enzyme, and INF-γ) after than before treatment among the studied patients indicate significant improvement in patients who received oral bLF 3 months
other↑, The results of this trial indicate that oral bLF made a significant increase in serum LF levels of patients in the test group 3 months after treatment compared to patients in the control group (P ≤ 0.05).
*ROS↓, Iron is essential as a catalyst for the production of reactive oxygen species. Therefore, lactoferrin can diminish the harmful influence of reactive oxygen species produced by leukocytes at the sites of inflammation
Imm↑, This result indicates that oral bLF enhances the immune system of colorectal cancer patients.
WBC↑, As a result of this increase in WBCs and neutrophil count patients disease state may be improved, because the body immune system can fight the disease more efficiently compatible with some previous studies
Neut↑,
T-Cell↑, These results support the proposal that oral supplements of bovine lactoferrin may be a useful adjunct toward modulation of immune activity, in particular T-cell activation and antioxidant status
*antiOx↑, The effect of antioxidants such as LF increase intracellular glutathione (GSH) levels in vascular endothelial cells by modulation of the GSH redox
*GSH↑,
*chemoP↑, On the other hand, oral bLF administration decreased chemotherapy related side effects as it enhances both renal and hepatic function tests.
*RenoP↑, Also, LF decreased chemotherapy related side effects by protecting liver and kidney from toxicity and improving their function test values
*hepatoP↑, Oral lactoferrin may increase liver functions and protect it from damage by reactive oxygen species since LF can function as an antioxidant, reducing intracellular levels of ROS
BUN↓, mean serum BUN decreased from 16.23 mg/dL before treatment to 11.43 mg/dL after 3 months of treatment in patients in the test group
creat↓, This decrease in BUN and serum creatinine may be due to the antioxidant effect of LF as mentioned in a former preclinical study on rat model of ferric nitrilotriacetate- (Fe-NTA-) induced renal tubular oxidative injury.
ALAT↓, Also, there was a significant decrease in serum ALT and AST in patients in test group 3 months after treatment compared to patients in the control group
AST↓,
RBC↑, Oral bLF administration enhanced anemia which is a very common chemotherapy related side effect; as results have shown, there were significant increases in RBCs count and serum Hb in patients in test group 3 months after treatment compared to patient
PC↑, There was a significant increase in platelets count in patients in test group after 3 months compared to control group
Mucositis↓, Patients in test group had less severed mucositis than patients in control group after every chemotherapy cycle;
*AntiBio↑, As mentioned before, lactoferrin has protective effects that range from direct antimicrobial activities against a large panel of microorganisms, including bacteria, viruses, fungi, and parasites, to anti-inflammatory and anticancer activities [
*AntiViral↑,
*AntiFungal↑,
*Inflam↓,
*antiOx↑, its role as health-promoting effect is attributed because it is rich source of antioxidant.
P53↑, anticancer management through the modulation of various molecular pathways including p53, pTEN, NF-κB, PI3K/Akt, Bcl-2, and VEGF
PTEN↑, figure 2
NF-kB↓,
PI3K↓,
Akt↓,
Bcl-2↓,
VEGF↓,
*Inflam↓, Neem also plays role as anti-inflammatory via regulation of proinflammatory enzyme activities including cyclooxygenase (COX), and lipoxygenase (LOX) enzyme.
*COX2/PTGS2↓,
*5LO↝,
*Wound Healing↑, figure 1
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
*AntiViral↑,
*Bacteria↑,
*AntiBio↑,
*AntiFungal↑,
cMyc↓, figure 2
BAX↓,
IAP1↓, Nimbolide downregulated cell survival proteins, including I-FLICE, cIAP-1, cIAP-2, Bcl-2, Bcl-xL, survivin, and X-linked inhibitor of apoptosis protein, and upregulated the proapoptotic proteins p53 and Bax
IAP2/BIRC3↓,
Bcl-xL↓,
survivin↓,
XIAP↓,
angioG↓, ethanolic fraction of neem leaf (EFNL) treatment effectively inhibited the expression of proangiogenic genes,
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
AD, |
NA |
|
|
|
*other↝, Nimbolide is one of the most potent limonoids derived from the flowers and leaves of neem (Azadirachta indica), which is widely used to treat a variety of human diseases.
*Inflam↓, Nimbolide has anti-inflammatory, anti-microbial, and anti-cancer properties, which make it an intriguing compound for research.
AntiCan↑,
*Bacteria↓, pharmacological properties including antimalaria, antibacterial, antiviral, antioxidative, anti-inflammatory, antiinvasive, neuroprotective, hepatoprotective, and pro-apoptotic properties
*AntiViral↑,
*neuroP↑,
*hepatoP↑,
*ROS?, Inhibit oxidative stress, Activate Nrf2/HO-1 signaling
*NRF2↑,
*HO-1↑,
*TLR4↓, Inhibit oxidative stress Anti-inflammatory and antioxidant TLR4/NF-κB signaling pathway
*NF-kB↓,
*AChE↓, down regulation of AChE and Aβ GSK-3β interaction
*Aβ↓,
*GSK‐3β↓,
*LDL↓, Nimbolide reduced intracellular cholesterol, free fatty acids, and triglycerides and enhanced hepatocyte function by inhibiting oxidative DNA damage and lipid peroxidation through its antioxidant effects
*DNAdam↓,
*lipid-P↓,
*antiOx↑, Nimbolide showed immense antioxidant properties.
*SOD1↑, nimbolide treatment increased superoxide dismutase (SOD-1), Nrf-2, GSH, and HO-1 protein expression
*GSH↑,
*IL6↓, Nimbolide treatment resulted in a reduction of the inflammatory cytokines IL-6, IL-1β, and TNF-α, as well as inflammatory cellular signaling molecules IkB-α, STAT3, and NF-kB.
*IL1β↓,
*STAT3↓,
*GPx↑, Glutathione peroxidase, catalase (CAT), concentration were all found to be up, while malondialdehyde and nitric oxide levels were shown to be significantly reduced by nimbolide.
*Catalase↑,
*MDA↓,
*AntiDiabetic↑, Anti-diabetic effect of nimbolide in diabetes
*HDL↓, suppression of the levels of pro-inflammatory mediators, (cholesterol, TG, LDL, and HDL, MCP-1, VEGF, and MMP-9)
*MCP1/CCL2↓,
*VEGF↓,
*MMP9↓,
*GutMicro↑, nimbolide showed to reduce inflammation, oxidative stress, and to reverse gut microbiota, which protects them from gestational diabetes.
TumCP↓, Nimbolide reported to decrease cell proliferation, EMT, cell cycle progression, and migration, in breast cancer cells via downregulating the NF-κB pathway
TumCCA↑,
TumCMig↓,
NF-kB↓,
ROS↑, nimbolide stimulates the overproduction of ROS, consequently modulating both autophagy and apoptosis in pancreatic cancer cells.
PI3K↓, nimbolide-induced ROS generation hindered cell proliferation by suppressing PI3K/AKT/mTOR and ERK signaling pathways.
Akt↓,
mTOR↓,
ERK↓,
EMT↓, nimbolide-mediated ROS generation reduced EMT, migration, colony forming abilities and invasion, thereby inhibiting metastasis.
TumMeta↓,
ChemoSen↑, use of nimbolide in combination with 5-FU showed a higher inhibitory rate in breast cancer than 5-FU alone
eff↑, nimbolide synergized the effect of TRAIL to induce apoptosis in tumor cell lines, but not normal breast cells
selectivity↑,
CDK4↓, slows tumor growth by inhibiting CDK4/6 activity
CDK6↓,
Wnt↓, nimbolide suppressed the Wnt/β-catenin signaling pathway mediated by NF-κB in HCC and pancreatic cancer cells
β-catenin/ZEB1↓,
STAT3↓, nimbolide can significantly suppress the activation of oncogenic transcription factor STAT3.
MMP2↓, inhibits tumor cell growth and migration by downregulating VEGF-A and MMP-2/9 expression,
Sp1/3/4↓, nimbolide inhibited MMP-9 activity by inhibiting the binding activity of Sp-1, AP-1 and NFk-B motifs, all of which are important transcription factors.
AP-1↓,
P21↑, Nimbolide exhibited dose-dependent inhibitory effects on HeLa cell viability by causing cell cycle arrest at G0/G1 phase with p53-dependent accumulation of p21.
*AntiArt↑, The findings of the study suggest that nimbolide has the ability to reduce the severity of rheumatoid arthritis by suppressing the expression levels of toll-like receptors, IL-23, IL-17, IFN-γ and HSP70.
*IL23↓,
*IL17↓,
*IFN-γ↓,
*HSP70/HSPA5↓,
| - |
Review, |
Nor, |
NA |
|
|
|
- |
Review, |
IBD, |
NA |
|
|
|
*antiOx↑, Rutin is a highly potent molecule due to its strong antioxidant properties
*antiAll↑, antiallergic [21] , anti-inflammatory and vasoactive [22] , antitumor [23] , antibacterial, antiviral, and antiprotozoal properties
*Inflam↓,
*AntiTum↑,
*Bacteria↓,
*AntiViral↑,
*BioAv↓, The major disadvantage associated with this molecule is poor solubility in aqueous media, being the reason for its poor bioavailability.
*AntiArt↑, Antiarthritic activity
*PLA2↓, rutin inhibited PLA2 activity, the initial enzyme in arachidonic acid cascade, from human synovial fluid
*chemoP↑, Rutin pretreatment prevented deteriorative effects induced by cisplatin through a protective mechanism that involved reduction of increased oxidative stress as well as caspase-3, TNF-a and NF-kB protein expression levels.
*ROS↓,
*Casp3↓,
*TNF-α↓,
*NF-kB↓,
*cardioP↑, Recent studies have shown the protective effect of rutin in various cardiovascular disorders such as hypertension, hyperlipidemia and myocardial infarction
*Stroke↓, The protective effects of rutin in myocardial infarction could be due to free radical scavenging activity, improving of multienzyme activities such as Na + /K + ATPase and Mg 2+ -ATPase and Ca 2+ -ATPase
*TG/TAG↓, Rutin significantly lowered levels of cholesterol, TGs, free fatty acids (FFAs), LDL-C, and VLDL-C in serum and increased the level of HDL-C in serum in ISO-treated rats (
*FFA/NEFA↓,
*LDL↓,
*HDL↑,
*AntiDiabetic↑, Rutin acts as an antidiabetic agent in several ways by enhancing the release of insulin from islets of langerhans,
*MPO↓, Rutin has shown to be effective in treatment of IBD due to its anti-inflammatory effects, which involve reduction in myeloperoxidase activity and inhibition of TNF-a-induced NF-kB activation in human colon cells and expression of IL-1b
*NF-kB↓,
*BioAv↓, The oral bioavailability of pure rutin is around 20%
*BioAv↝, Common approaches used to enhance bioavailability of rutin are particle diminution to the submicron range and by complexation of rutin with cyclodextrins and various metals.
*AntiBio↑, TQ, have a broad antimicrobial spectrum including Gram-negative, Gram-positive bacteria, viruses, parasites, schistosoma and fungi.
*AntiViral↑,
*AntiFungal↑,
Inflam↓, Ursolic acid has been shown to target multiple proinflammatory transcription factors, cell cycle proteins, growth factors, kinases, cytokines, chemokines, adhesion molecules, and inflammatory enzymes.
TumCCA↑,
chemoPv↑, potentially mediate the chemopreventive and therapeutic effects of ursolic acid by inhibiting the initiation, promotion and metastasis of cancer.
TumMeta↓,
antiOx↑, Numerous biochemical and pharmacological effects of ursolic acid, including anti-inflammatory, antioxidant, antiproliferative, anticancer, antimutagenic, antiartherosclerotic, antihypertensive, antileukemic, antiviral, and antidiabetic, have been rep
AntiViral↑,
AntiDiabetic↑,
Showing Research Papers: 1 to 40 of 40
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 40
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
ASAP2↓, 1, CDK7↓, 1, LRIG1↑, 1, MTA1↓, 1, Mucositis↓, 2, PC↑, 1, RBC↑, 1, SUMO↓, 1, WBC↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 2, Catalase↓, 1, Catalase↑, 1, Ferroptosis↑, 1, GPx4↓, 1, GSH↓, 4, lipid-P↑, 3, MDA↑, 1, MFN2↑, 1, NRF2↓, 1, NRF2↑, 1, PARK2↑, 1, ROS↓, 3, ROS↑, 13, ROS⇅, 1, mt-ROS↑, 1, SOD↓, 1, SOD↑, 1, TAC↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 2, ETC↓, 1, MEK↓, 1, MMP↓, 7, mtDam↓, 1, mtDam↑, 2, PINK1↑, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, AMPK↑, 1, BUN↓, 1, cMyc↓, 3, Glycolysis↓, 1, SIRT1↓, 2,
Cell Death(tgid=5) ⓘ
Akt↓, 8, Akt↑, 1, p‑Akt↓, 2, Apoptosis↑, 12, BAD↑, 1, Bak↑, 1, BAX↓, 1, BAX↑, 6, Bax:Bcl2↑, 2, Bcl-2↓, 6, Bcl-xL↓, 2, Casp3↑, 6, cl‑Casp3↑, 2, cl‑Casp3⇅, 1, proCasp3↓, 1, Casp7↑, 2, cl‑Casp7↑, 1, Casp8↑, 1, Casp9↑, 3, cl‑Casp9↑, 2, Cyt‑c↑, 6, Fas↑, 1, Ferroptosis↑, 1, hTERT/TERT↓, 1, IAP1↓, 2, IAP2/BIRC3↓, 1, iNOS↓, 1, JNK↓, 1, p‑JNK↑, 1, MAPK↑, 2, MAPK↝, 1, p‑MAPK↓, 1, Mcl-1↓, 2, p27/CDKN1B↑, 1, p38↓, 1, p38↑, 2, p‑p38↑, 1, Paraptosis↑, 1, survivin↓, 4, TumCD↑, 2,
Kinase & Signal Transduction(tgid=6) ⓘ
miR-25-5p↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
miR-21↓, 1, other↑, 1, other↝, 2, tumCV↓, 3,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 3, HSP90↓, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
ATG5↑, 1, Beclin-1/ATG6↑, 2, LC3II↑, 2, MitoP↑, 1, p62↓, 1, TumAuto↑, 5,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 3, DNMT3B↓, 2, P53↓, 1, P53↑, 6, P53↝, 1, PARP↑, 2, cl‑PARP↑, 6, PCNA↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK4↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 4, mitA↑, 1, P21↑, 1, TumCCA↑, 14,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
p‑cDC2↓, 1, CSCs↓, 1, EMT↓, 3, ERK↓, 3, p‑ERK↓, 1, GSK‐3β↑, 2, mTOR↓, 5, mTOR↝, 1, p‑mTOR↓, 2, mTORC1↓, 1, NOTCH↓, 1, P70S6K↓, 1, PI3K↓, 6, PTEN↑, 2, STAT↓, 1, STAT3↓, 5, p‑STAT3↓, 1, TumCG↓, 4, Wnt↓, 2,
Migration(tgid=13) ⓘ
AP-1↓, 1, BACH1↓, 1, CD31/PECAM-1↓, 1, CLDN1↑, 1, E-cadherin↑, 1, fascin↓, 1, LAMs↓, 1, LRP1↓, 1, MMP2↓, 4, MMP9↓, 3, MMPs↓, 3, N-cadherin↓, 1, Smad1↓, 1, TGF-β↓, 2, TIMP1↑, 2, TIMP2↓, 1, TJ↑, 1, TumCI↓, 4, TumCMig↓, 3, TumCP↓, 10, TumMeta↓, 5, TumMeta↑, 1, ZO-1↑, 1, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 8, angioG↑, 1, EGFR↓, 2, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 3, VEGF↓, 8,
Barriers & Transport(tgid=15) ⓘ
BBB∅, 1, GLUT4↓, 1, IBI↑, 1, OCLN↑, 1, P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 3, IL1β↓, 2, IL6↓, 2, IL8↓, 1, Imm↑, 2, Imm↝, 1, INF-γ↝, 1, Inflam↓, 1, JAK↓, 1, MyD88↑, 1, Neut↑, 1, NF-kB↓, 6, NK cell↑, 2, PD-1↓, 1, PD-L1↓, 1, T-Cell↑, 1, TLR4↓, 1, TLR4↑, 1, TNF-α↓, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 2, BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 8, Dose↝, 9, eff↓, 3, eff↑, 15, Half-Life↑, 1, MDR1↓, 1, RadioS↑, 1, selectivity↑, 3,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, creat↓, 1, EGFR↓, 2, GutMicro↑, 1, hTERT/TERT↓, 1, IL6↓, 2, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 11, AntiDiabetic↑, 1, antiNeop↑, 2, AntiTum↑, 4, chemoP↑, 1, chemoPv↑, 1, fatigue↓, 1, fatigue∅, 1, NP/CIPN↓, 1, OS↑, 1, QoL∅, 1, Risk↓, 2, toxicity↓, 2, toxicity↝, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 3,
Total Targets: 221
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
antiAll↑, 1, AntiArt↑, 3, AntiBio↑, 7, antiD↓, 1, AntiP↓, 1, AntiP↑, 1, diuretic↑, 1, FFA/NEFA↓, 1, PLA2↓, 1, Stroke↓, 4, TRPA1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, antiOx↑, 19, ARE↑, 1, Catalase↑, 6, GPx↑, 5, GSH↑, 5, HDL↓, 1, HDL↑, 1, HO-1↓, 1, HO-1↑, 4, Keap1↝, 1, lipid-P↓, 3, MDA↓, 4, MPO↓, 1, NQO1↑, 1, NRF2↑, 6, ROS?, 1, ROS↓, 9, ROS↑, 1, mt-ROS?, 1, SIRT3↑, 1, SOD↑, 5, SOD1↑, 1, TAC↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↓, 1, ATP↑, 2, Insulin↑, 1, MMP↑, 1, PGC-1α↝, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 2, AMPK↑, 1, BUN↓, 1, cAMP↑, 1, glucose↓, 2, LDL↓, 3, NADPH↓, 1, NADPH↑, 2, PPARγ↓, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Apoptosis↓, 1, BAX↓, 1, Bcl-2↑, 1, Casp3↓, 3, Casp9↓, 1, GSDMD↓, 1, JNK↓, 1, JNK↑, 1, MAPK↓, 3,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, AntiThr↑, 4, cJun↓, 1, other↝, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↑, 1, cl‑eIF2α↑, 1, GRP78/BiP↑, 1, HSP70/HSPA5↓, 1, HSP70/HSPA5↑, 1, p‑PERK↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1/ATG6↑, 1, LC3II↑, 1, p62↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, importin α/β↓, 1, PARP1↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 2, GSK‐3β↓, 3, HDAC2↓, 1, mTOR↓, 1, mTOR↑, 1, PI3K↓, 1, PI3K↑, 1, STAT3↓, 1, STAT3↑, 1, STAT5↓, 1,
Migration(tgid=13) ⓘ
5LO↝, 1, AP-1↓, 1, MMP9↓, 2, PAI-1/SERPINE1↓, 1, PTP1B↓, 1, VCAM-1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
eNOS↑, 1, NO↓, 2, NO↑, 2, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 4,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, COX2/PTGS2↑, 1, ICAM-1↓, 1, IFN-γ↓, 1, IL17↓, 1, IL18↓, 1, IL1β↓, 5, IL23↓, 1, IL4↓, 1, IL6↓, 5, Imm↑, 4, Imm⇅, 1, Inflam↓, 27, Inflam↑, 1, pol-M2 MC↑, 1, MCP1/CCL2↓, 1, MUC2↓, 1, NF-kB↓, 8, NK cell↑, 1, PGE2↓, 2, PGE2↑, 1, TLR4↓, 1, TNF-α↓, 6, TNF-α↑, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 4, BDNF↑, 2, NGF↑, 1, tau↓, 1, p‑tau↓, 3, TrkB↝, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 4, BACE/β-secretase↓, 1, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 6, BioAv↑, 7, BioAv↝, 3, Dose↝, 3, eff↑, 6, eff↝, 2, Half-Life↓, 1, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 2, AST↓, 2, GutMicro↑, 4, IL6↓, 5, MUC19↓, 1, TG/TAG↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 3, AntiCan↑, 3, AntiDiabetic↑, 13, antiPs↑, 1, AntiTum↑, 3, Bone Healing↑, 1, cardioP↑, 10, chemoP↑, 3, cognitive↑, 4, hepatoP↑, 8, memory↑, 2, neuroP?, 1, neuroP↑, 13, Obesity↓, 3, RenoP↑, 4, toxicity↓, 6, toxicity↑, 2, toxicity↝, 3, Wound Healing↑, 3,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 9, AntiViral↑, 37, Bacteria↓, 16, Bacteria↑, 1, Diar↓, 1, Sepsis↓, 1,
Total Targets: 171
Scientific Paper Hit Count for: AntiViral, AntiViral
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1381 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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