TAC Cancer Research Results
TAC, total antioxidant capacity: Click to Expand ⟱
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Total antioxidant capacity (TAC) refers to the ability of a biological sample (such as blood, tissues, or food) to counteract oxidative stress by neutralizing free radicals and reactive oxygen species (ROS).
May have reduced levels in cancers.
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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.
*ROS↓, At 96 h after culture, a decrease in ROS and an increase in TAC were observed in ALA group compared to control group (p < 0.05).
*TAC↑,
*eff↑, ALA (100 uM) improves the in vitro development of follicles. This effect may be mediated by decreasing ROS concentration and increasing follicular TAC level during the culture period.
*SOD↑, ALA administration significantly elevated plasma total antioxidant status and could increase activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in the brain tissues of male rat exposed to restraint stress
*GPx↑,
*Catalase↑,
*GlucoseCon↑, ALA enhances glucose uptake by cells,
*antiOx↑, Taken together, our study indicates that ALA has an excellent antioxidant activity,
*Inflam↓, Phyllanthus emblica polysaccharides (PEP) exhibit anti-inflammatory, antioxidant, and gut microbiota-modulating properties in colitis and obese mice.
*antiOx↓,
*GutMicro↑,
*cognitive↑, In vivo results showed that PEP administration significantly alleviated cognitive decline by reducing neuroinflammatory cytokines (TNF-α, IL-6, and IL-1β) and MDA levels while increasing anti-inflammatory factors (IL-4 and IL-10) and antioxidants (S
*TNF-α↓,
*IL6↓,
*IL1β↓,
*MDA↓,
*IL4↑,
*IL10↑,
*TAC↑,
*ATG5↑, Mechanistically, PEP upregulated autophagy-related proteins (Atg5, Beclin1, and LC3B) and LRP1 expression while downregulating AD-related proteins (BACE1, APP, Aβ, and phospho-TauSer404)
*Beclin-1/ATG6↑,
*LC3B↑,
*LRP1↑,
*BACE/β-secretase↓,
*APP↓,
*Aβ↓,
*tau↓,
*Dose↝, four cows sequentially supplemented fresh amla fruit (FAF) at three levels (200, 400, then 600 g/d) (treatment group) at 14-day intervals.
*TAC↑, amla fruit increased the antioxidant capacity biomarkers in the blood, such as superoxide dismutase (SOD) and albumin; this confirms that amla fruit is an excellent antioxidant, inhibiting reactive oxygen species’ (ROS) metabolism,
*SOD↑,
*Albumin↑,
*ROS↓,
*other↑, fresh amla fruit doses for lactating cows at 400 g/d on an as-fed basis can be used as an alternative additive feed in dairy cow diets to improve antioxidant capacity, protein efficiency, butter quality, and to produce more desirable milk fatty acid
*hepatoP↑, promoting the recovery of liver function in mice with liver fibrosis.
*PKM2↓, API inhibits the transition of Pyruvate kinase isozyme type M2 (PKM2) from dimer to tetramer
*Hif1a↓, blocking PKM2-HIF-1α access
*MDA↓, leads to a decrease in malondialdehyde (MDA) and Catalase (CAT) levels and an increase in glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) levels, as well as total antioxidant capacity (T-AOC) in the liver of mice
*Catalase↓,
*GSH↑,
*SOD↑,
*GPx↑,
*TAC↑,
*α-SMA↓, API downregulated the expression of α-smooth muscle actin (α-SMA), Vimentin and Desmin in the liver tissue of mice with liver fibrosis
*Vim↓,
*ROS↓, API can inhibit HSC activation and alleviate CCl4 induced liver fibrosis by inhibiting the PKM2-HIF-1α pathway and reducing oxidative stress,
*memory↑, BA significantly improved learning and memory impairments induced by AlCl3 treatment.
*AChE↓, BA treatment significantly decreased acetylcholinesterase levels and reduced amyloid-beta (Aβ) expression
*Aβ↓,
*TNF-α↓, BA ameliorated the increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), inhibited lipid peroxidation, and increased total antioxidants in the brain.
*IL1β↓,
*lipid-P↓,
*TAC↑,
*BDNF↑, Indeed, BA significantly suppressed AlCl3-induced decrease of brain-derived neurotrophic factor, pGSK-3β (Ser 9), and β-catenin.
*β-catenin/ZEB1↑,
*Dose↑, BA (250 mg/kg) showed a significant protective effect compared to a lower dose.
*ROS↓, TBSE could successfully inhibit H2O2-induced ROS overproduction, restore and balance the mitochondrial membrane potential, while also significantly increasing cellular antioxidant activity (CAA) and the expression of protective enzymes such as SOD,
*MMP↑,
*TAC↑,
*SOD↑, expression of protective enzymes such as SOD, CAT, and GST.
*Catalase↑,
*GSTA1↑,
*NRF2↑, TBSE triggered the translocation of Nrf2
*NQO1↑, treatment of cells with TBSE and quercetin markedly increased the expression of NQO1, HO-1, and total Nrf2
*HO-1↑,
*Imm↑, CA enhances immune responses, reduces inflammation, exerts antimicrobial effects, and improves overall fish health.
*Inflam↓,
*Bacteria↓,
*eff↑, sustainable functional-feed strategies that diminish antibiotic reliance in aquaculture.
*ROS↓, Reduced MDA levels and ROS accumulation
*MDA↓,
*Catalase↑, Increased CAT, GSH, and T-AOC activities
*GSH↑,
*TAC↑,
*NF-kB↓, Suppressed the activation of the NF-κB signaling pathway and the NLRP3 inflammasome pathway in the gills
*NLRP3↓,
*eff↑, In rainbow trout (Oncorhynchus mykiss), co-supplementation with 1–3 g RA/kg and Lactobacillus rhamnosus yielded synergistic improvements in growth, antioxidant capacity, and stress tolerance
*AST↓, In rainbow trout, CinA (0.25–1.5 g/kg) lowered intestinal pH, serum triglycerides, and hepatic enzyme levels (AST and ALT), while upregulating hepatic antioxidant genes (SOD and GST) [49]
*ALAT↓,
*SOD↑,
*GSTA1↑,
*NRF2↑, CA activated nuclear factor erythroid 2-related factor 2 (Nrf2) and inhibited nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1), leading to increased antioxidant enzyme activity and reduced intracellular ROS levels.
*NOX↓,
*TAC↑,
*ROS↓, CA reduces intracellular ROS via Keap1/Nrf2 signalling and increases antioxidant enzyme expression
*NQO1↑, CA treatment enhanced the expression of Nrf2 (Figs. 4C and F), and the content of NQO1
*p‑PTEN↑, CA intervention significantly upregulated p-PTEN expression
RUNX2↓, CA inhibits the expression of Runx2 and SOX9
SOX9↓,
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*Inflam↓, anti-inflammatory, antioxidant, and AChEI properties
*antiOx↑,
*AChE↓,
*BBB↑, Carvacrol is able to cross the blood brain barrier easily, notably improving its therapeutic efficacy in neurodegenerative disorders
*cardioP↑, prevention of many chronic diseases, such as cancer as well as infectious, cardiovascular and neurodegenerative diseases
*neuroP↑, Extensive researches have revealed carvacrol neuroprotective properties
*memory↑, memory-enhancing activities
*TAC↑, Carvacrol has antioxidant activity and was shown to act as a dietary phyto-additive to boost animal antioxidant status (sharifi-Rad et al., 2018
*ROS↓, carvacrol could protect neuronal injuries against Aluminum-induced oxidative stress leading to lipid peroxidation
*lipid-P↓,
*MDA↓, carvacrol has been indicated to reduce malondialdehyde (MDA) and neuronal cell necrosis, and increase superoxide dismutase (SOD) and catalase (CAT) activity levels in the hippocampus (
*SOD↑,
*Catalase↑,
*NRF2↑, carvacrol activated nuclear factor-erythroid 2-related factor 2 (Nrf2) as an endogenous antioxidant
*cognitive↑, Carvacrol administration (25, 50, and 100 mg/kg) during 21 days attenuated memory impairments and enhanced cognition compared to the control group.
*IL1β↓, Carvacrol administration diminished the expression of interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α).
*COX2/PTGS2↓,
*TNF-α↓,
*TLR4↓, carvacrol could significantly decrease Toll-like receptor 4 (TLR4) and increase brain-derived neurotrophic factor (BDNF) expression.
*BDNF↑,
*PKCδ↑, carvacrol and thymol might have protective ability on cognitive function in AD by activation of PKC pathway
*5LO↓, Carvacrol inhibited AChE and lipoxygenase activity that supports its anti-inflammation and anti-Alzheimer effects
*TRPM7↓, Reduced caspase-3 levels, and TRPM7 channels inhibitor
*GSH↑, Antioxidant activity, Increased glutathione
*other↑, revealed a remarkable neuroprotective action of carvacrol in cerebral ischemia in animal models
*Ferroptosis↓, via ferroptosis inhibition by elevating GPx4 expression
*GPx4↑,
AntiCan↑, Chlorogenic acid (5-caffeoylquinic acid, CGA), found in plants and vegetables, is promising in anticancer mechanisms.
*chemoP↑, CGA can overcome resistance to conventional chemotherapeutics and alleviate chemotherapy-induced toxicity by scavenging free radicals effectively.
TNF-α↓, CGA reduces inflammation levels in renal tissues by down-regulating tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2),
COX2/PTGS2↓,
IL6↓, Moreover, CGA exhibits a protective effect against 5-FU-induced ovarian tissue damage, reducing Interleukin 6 (IL-6) levels;
eff↑, CGA suppresses the expression of Programmed Cell Death Ligand 1 (PD-L1) on cancer cells, boosting the antitumor effect of the anti-PD-1 antibody and enhancing anticancer immunotherapy
PD-L1↓,
*cognitive↓, CGA, have shown promise in preventing cognitive dysfunction and suppressing amyloid β plaques
*Aβ↓,
*TAC↑, hyperlipidemic patients who ingested 200 mL of Mate tea (12.5 mg/mL) daily experienced a significant increase in serum total antioxidant status and the enzymatic activity of superoxide dismutase (SOD),
*SOD↑,
*eff↑, In blueberry jam production, the high-temperature processing of blueberries with sucrose promoted the formation of 11 CGA derivatives
*eff↑, roasting process (170 to 200 °C/10 to 30 min) of coffee beans promotes CGA transformation to four chlorogenic acid lactones
ChemoSen↑, CGA was found to increase the sensitivity of hepatocellular carcinoma cells to 5-FU treatment
tumCV↓, CGA was shown to collaborate by significantly reducing cell viability and growth through induction of apoptosis, attributed to inhibition of extracellular signal-regulated kinases (ERKs)
Apoptosis↑,
ERK↓,
chemoP↑, Protective Role of Chlorogenic Acid against Toxicity Induced by Chemotherapy
*GPx↑, figure4
*GSTs↑,
*GSH↑,
*SOD↑,
*Catalase↑,
*ROS↓,
*lipid-P↓,
*MDA↓,
*Casp3↓,
*HO-1↓,
cardioP↑, reported the cardioprotective effect of CGA against doxorubicin-induced cardiotoxicity in female Swiss albino mice.
radioP↑, The radioprotective potential of CGA against γ-radiation-induced chromosomal damage in male albino Swiss mice was initially demonstrated in 1993.
*antiOx↑, Chicoric acid (CA) is a natural antioxidant with promising hepatoprotective activity.
*hepatoP↑,
*ROS↓, Pre-treatment with CA suppressed reactive oxygen species and lipid peroxidation and enhanced antioxidants in MTX-induced rats.
*lipid-P↓,
*TAC↑,
*NRF2↑, CA upregulated hepatic Nrf2, HO-1, NQO-1, and PPARγ, and attenuated inflammation.
*HO-1↑,
*NQO1↑,
*PPARγ↑,
*Inflam↓,
*Apoptosis↓, CA inhibited apoptosis by increasing Bcl-2 expression and suppressing Bax, cytochrome c, and caspase-3 in MTX-administered rats.
*Bcl-2↑,
*BAX↓,
*Cyt‑c↓,
*Casp3↓,
*ALAT↓, D-carvone significantly enhanced liver functions (ALT, AST), oxidant/antioxidant
status (MDA, SOD, GSH, total antioxidant capacity; TAC), as well as histopathological changes.
*AST↓, administration with D-carvone (50 mg/kg, bw) significantly reduced serum ALT and AST to 54.8% and 51% compared to the CCl4 model group, respectively
*MDA↓, decreased the MDA levels to 50.7%, while it restored the depleted GSH and SOD
levels to 233% and 221.5%, respectively
*SOD↑,
*GSH↑,
*TAC↑,
*eff↑, D-carvone effectively attenuated the progression of liver fibrosis, evident by the decreased collagen deposition and fibrosis score by Masson trichrome staining (MT) and α-SMA protein expression
*TGF-β1↓, significant downregulation of the pro-fibrogenic markers TGF-β1 and SMAD3 and upregulation of MMP9.
*SMAD3↓,
*MMP9↑,
*NRF2↑, D-carvone promotes the Nrf2 signaling pathway which might contribute to the antioxidative activity of D-carvone
*antiOx↑,
*hepatoP↑,
*Inflam↓, D-carvone administration appreciably reduced the inflammatory cells’ infiltration and pro-inflammatory modulators release provoked by liver injury
*NF-kB↓, D-carvone include downregulation of NF-κB
*NO↓, D-carvone has been reported to diminish the excessively produced NO by macrophages and Kupffer cells in the injured liver
*cAMP↑, carvone has been found to activate the cyclic adenosine monophosphate (cAMP) signaling pathway
*ROS↓, by Inhibiting Oxidative Stress
NF-kB↓, NF-Kβ suppression from Cur interaction led to the identification of Cur’s immunomodulatory effects
Imm↑, on various cytokines and immune related proteins such as IL-6, TNF-α, and PD-L1 and is suggested as a potential adjuvant treatment for immunotherapy
*TAC↑, In clinical trials, Cur is shown to increase total antioxidant capacity (TAC) and decrease malondialdehyde.53
*MDA↓,
ROS↑, increases overall ROS accumulation in SiHa cervical cancer cells resulting in increased autophagy and G2/M phase cell cycle arrest.54
TumAuto↑,
TumCCA↑,
Keap1↑, activate KEAP1/NRF2/ARE pathways and serve as an effective therapeutic especially in combination with 5-FU
ChemoSen↑,
ER Stress↑, administration of 1g resulted in ROS production, G1 cell cycle phase arrest, and increased ER-stress which was reversed upon addition of NAC, an ROS scavenging agent
eff↓, reversed upon addition of NAC
TrxR↓, Non-small cell lung cancer cell lines showed marked increases in apoptosis and ferroptosis driven by the analogs ability to generate ROS through TrxR inhibition.
STAT3↓, analog WZ26 increased ROS and cell death in cholangiocarcinoma via STAT3 inhibition
*BioAv↓, Studies with doses as high as 12 g/day still resulted in small amounts of traceable plasma Cur, mostly due to low absorption in the small intestine and rapid elimination in the body via the gall bladder.
*antiOx↑, Curcumin is an antioxidant agent with both radiosensitizing and radioprotective properties
radioP↑,
RadioS∅, In the present study we have failed to observe any radiosensitizing or prooxidant feature for curcumin in the prescribed dose;
*TAC↑, The present study showed that curcumin can increase TAC and decrease SOD activity in the plasma of patients with prostate cancer receiving radiotherapy; these observations are thought to be possibly brought about by the antioxidant effect of curcumin
*SOD↓, 3 mo after completion of radiotherapy, TAC increased significantly (P < 0.001) and the activity of
SOD decreased significantly
*Dose↝, 180 mg of EA per day (n = 22) or a placebo (n = 22) for 8 weeks
*MDA↓, we saw a significant decrease and increase in the MDA and TAC in the intervention group
*TAC↑,
*CRP↓, EA consumption reduced CRP and IL-6 levels, and these changes were significant in comparison with placebo group changes
*IL6↓,
*Inflam↓, EA, may help maintain intestinal health by modulating inflammation and oxidative stress and ultimately improving the quality of life in IBS patients.
*ROS↓,
*QoL↑,
*toxicity↓, In this study, we did not receive any adverse effects reports from patients about EA consumption.
*Copper↓, AE treatment decreased copper accumulation and regulated Aβ metabolism in the brain of model rats, thereby improving Aβ deposition, memory impairment, hippocampal nerve cell damage, and related biochemical indicators.
*Aβ↓, AE Reduces the Deposition of Aβ in Hippocampus of AD-like Model Rats
*memory↑,
*cognitive↑, AE Inhibits the Cognitive Impairment of AD-like Model Rats
*Apoptosis↓, AE Ameliorates Neuronal Apoptosis in Hippocampus of AD-like Model Rats
*TAC↑, AE Improved the Antioxidant Capacity of AD-like Model Rats
*Inflam↓, AE Alleviated the Neuroinflammation in the Brain of AD-like Model Rats
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*AntiCan↑, (Eug), a volatile phenolic bioactive compound with a formula of C10H12O2, has been reported to have anticancer, antidiabetic, cardio‐ and pulmonary protective roles.
*AntiDiabetic↑,
*cardioP↑, Eugenol has been proven effective in modulating gut microbiota and attenuating adiposity in high‐fat diet‐fed C57BL/6J mice.
*toxicity↝, According to WHO, the safe dose of eugenol is 2.5 mg/kg for consumption
*GutMicro↑,
*neuroP↑, Moreover, it has the ability to improve gut health and prevent neurodegenerative disorders.
*BioAv⇅, Furthermore, multiple carriers like liposomes, glycodendritic polyamine dextran, solid lipid nanoparticles, and corn protein nanoparticles have been reported to deliver eugenol.
*BioAv↝, Eugenol (150 mg) in gelatin capsules was orally administered in healthy adults and absorbed very quickly, and ~55% is eliminated in urine after being transformed to glucuronic acid or eugenol sulfate conjugate in the liver
*antiOx↑, The studies on eugenol have proved its antioxidant and anti‐inflammatory properties.
*Inflam↑,
*AntiArt↑, aMateen et al. (2019) reported that eugenol alleviated arthritis via attenuating pro‐inflammatory cytokines (TNF‐α, IL‐6, IL‐10).
*TNF-α↓,
*IL6↓,
*IL10↓,
*GSH↑, Eugenol (2.5, 5, 10 mg/kg) improved GSH, GPx, and CAT levels while reducing carrageenan‐induced OS in arthritic rats (Adefegha et al. 2019).
*GPx↑,
*Catalase↑,
*MDA↓, reported reduced MDA and improved SOD, CAT, and TAC levels.
*TAC↑,
TumCMig↓, eugenol subdued cell migration and invasion by suppressing angiogenesis‐related protein expression and modulating JAK2/STAT3 pathways.
TumCI↓,
Akt↑, MDA‐MB‐231, SK‐BR‐3 ↑AKT, FOXO3a, Caspase‐3/9, p21
FOXO3↑,
Casp3↑,
Casp9↑,
P21↑,
angioG↓, Eugenol has been reported to reduce angiogenesis, inhibit invasion, and trigger apoptosis
TumCI↓,
Apoptosis↑,
NF-kB↓, GC via apoptosis induction, metastasis inhibition, downregulation of NF‐κB, and angiogenesis reduction is shown in Figure 3
eff↑, eugenol (153 μM) combined with 5‐fluorouracil proved effective in inhibiting cell growth and division in HeLa cells.
eff↑, eugenol (200–350 μM) with sulforaphane (6.5–8 μM) lowered the expressions of COX‐2, IL‐β, and Bcl‐2 and inhibited cell proliferation
ChemoSen↑, co‐treatment of eugenol and cisplatin reduced cell proliferation and induced apoptosis in G361 melanoma cells via inhibited MMP and proteasome activity,
NA↑, Eugenol proved effective in HL‐60 cell lines by inducing ROS‐mediated apoptosis with a 23.7 IC50 value
Casp3↑, eugenol‐induced apoptosis via ROS production and caspase‐9/3 activation.
Casp9↑,
*AntiDiabetic↑, Chilukoti et al. (2024) verified the antidiabetic activity of eugenol in rats.
*glucose↓, eugenol (400 mg/kg) significantly lowered glucose levels, reduced OS and inflammation, inhibited MDA levels, and improved GSH.
*ROS↓,
*Inflam↓,
*MDA↓,
*GSH↑,
*BioAv↑, Multiple delivery systems, such as liposomes, nanoparticles, nanoemulsions, and hydrogels, enhance its bioavailability, controlled release, and targeted delivery, making eugenol more effective for pharmaceutical and biomedical applications.
*Dose↝, group 3 received FA (100 mg/kg, orally)
*TAC↑, PQ administration increased plasma levels of biochemical parameters, decreased antioxidant enzymes activity, increased protein carbonyl and malondialdehyde (MDA) in serum and renal tissues (p˂0.05). FA administration after exposure to PQ improved all
*MDA↓,
*RenoP↑, This study demonstrates that daily consumption of FA can serve as an effective strategy to protect the kidneys from damage caused by chemical agents such as PQ.
*PI3K↓, This phenolic compound can inhibit the PI3K/Akt signaling pathway, reduce ROS, and invoke anti-inflammatory responses by modulating PPARγ and NF-κB expression
*Akt↓,
*ROS↓,
*Inflam↓,
PPARγ↝,
*NF-kB↓,
*IL6↓, FA effects against neuroinflammation are associated with decreased levels of pro-inflammatory cytokines such as IL-6, TNF-α, IL-1β (Bao et al. 2019) and inducible nitric oxide synthase (iNOS) in animal models
*TNF-α↓,
*iNOS↓,
*ALAT↓, Notably, co-administration of PQ and FA resulted in a significant reduction (p<0.001) in serum urea, Cr, uric acid, ALT, and AST levels
*AST↓,
*Urea↓,
*Catalase↑, we found that not only the enzymatic activity of CAT, SOD, and GPx increased, but also there was an elevation in the tissue levels of GSH
*SOD↑,
*GPx↑,
*GSH↑,
*antiOx↑, Molecular hydrogen (H2) has recently been recognized for its antioxidant and anti-inflammatory properties
*Inflam↓,
*ROS↓, inhaled H2 significantly reduced inflammatory cell infiltration, OS markers, and pro-inflammatory cytokine expression while upregulating antioxidant enzyme activity.
*TAC↑,
*IgE↓, Furthermore, H2 also significantly decreased serum IgE levels, a marker of allergic inflammation.
*Dose↝, 3% H2 gas inhalation on OVA-induced inflammatory airway conditions, body and lung weights were recorded in mice.
*NLR↓, Our results also demonstrated a significant decline in the NLR in the HT group compared to the NT group
*IL4↓, Conversely, the levels of IL-4 (p < 0.001; Figure 4A), IL-5 (p < 0.001; Figure 4B), IL-13 (p < 0.01; Figure 4C), and GM-CSF (p < 0.01; Figure 4F) were significantly lower in the HT group than in the NC group
*IL5↓,
*IL13↓,
*GM-CSF↓,
*NO↓, NO (p < 0.05; Figure 5B) levels were reduced in the HT group compared with those in the NC group
*GPx↑, treatment with 3% H2 significantly increased the GPx activity in the HT group compared to that in the NC group
*Eos↓, In our study, we observed that H2 inhalation reduced neutrophils in the OVA-induced asthmatic BALB/c mouse model
*TAC↑, The flavonoid hyperoside has been reported to elicit cytoprotection against oxidative stress partly by increasing the activity of antioxidant enzymes, such as glutathione peroxidase, superoxide dismutase and catalase.
*GPx↑,
*Catalase↑,
*ROS↓, by significantly inhibiting overproduction of intracellular ROS, depletion of the mitochondrial membrane potential and leakage of lactate dehydrogenase.
*MMP↓,
*LDH↑,
*HO-1↑, Hyperoside further enhanced the cellular antioxidant defense system through increasing the activity of heme oxygenase-1 (HO-1), and by up-regulating HO-1 expression
*NRF2↑, hyperoside stimulated nuclear translocation of the Nrf(2) transcription factor in a dose-dependent manner,
*radioP↑, In vitro, ISL restored the viability of X-ray-irradiated PC12 cells; reduced LDH release and intracellular ROS accumulation; and enhanced SOD1 activity, GSH content, and T-AOC levels.
*LDH↓,
*ROS↓,
*SOD1↑,
*GSH↑,
*TAC↑,
*NRF2↓, Moreover, ISL upregulated the expression of antioxidant-related genes and induced Nrf2 nuclear translocation.
*cognitive↑, In vivo, oral ISL administration ameliorated radiation-induced cognitive impairment, improved spatial learning and memory, alleviated hippocampal neuronal loss, and increased cerebral cortical Nrf2 expression in C57BL/6J mice
*Learn↑,
*memory↑,
*AGEs↓, Results demonstrated that ISV effectively inhibited AGEs formation in bovine serum albumin (BSA)-
*TAC↑, In C. elegans, ISV reduced AGEs accumulation, enhanced antioxidant capacity, and improved intestinal barrier function.
*IBI↑,
*TJ↑, upregulated tight junction proteins, and suppressed oxidative stress and apoptosis.
*ROS↓,
*Apoptosis↓,
AntiCan↑, kaempferol (a dietary flavonoid found abundantly in fruits, vegetables, and medicinal plants) has garnered significant attention for its promising anticancer properties.
TumCP↓, proliferation, invasion, inflammation, angiogenesis, oxidative stress, and apoptosis.
TumCI↓,
Inflam↓,
angioG↓,
ROS↑, kaempferol-induced apoptosis in HCT116 and SW480 cells involves reactive oxygen species (ROS) generation,
Apoptosis↑,
ChemoSen↑, kaempferol has shown the ability to reverse drug resistance, modulate epigenetic mechanisms, and enhance the efficacy of conventional chemotherapeutics, positioning it as a potential adjuvant therapy in CRC treatment.
Risk↓, diets abundant in fruits, vegetables, and phytochemicals appear to exert a protective effect
*antiOx↑, These include antioxidant, anti-inflammatory, antimicrobial, cardioprotective, neuroprotective, and notably, anticancer effects
*Inflam↓,
*AntiBio↑,
*cardioP↑,
*neuroP↑,
selectivity↑, One of the key features of kaempferol is its ability to selectively inhibit the growth of malignant cells while sparing or even protecting normal cells.
PUMA↑, kaempferol has been shown to increase the expression of p53-upregulated modulator of apoptosis (PUMA) and to trigger the release of cytochrome c from mitochondria
Cyt‑c↑,
cl‑Casp3↑, enhances the activation of caspase-3 and PARP cleavage, hallmarks of apoptosis
cl‑PARP↑,
Apoptosis↑,
NF-kB↓, nuclear factor kappa B (NF-κB), cyclooxygenase-2 (COX-2), and interleukin-6 playing pivotal roles in tumor promotion and immune evasion. Kaempferol effectively downregulates these pro-inflammatory mediators
COX2/PTGS2↓,
CC(CDKs/cyclins)↓, It inhibits cyclin-dependent kinases (CDKs), particularly CDK2, leading to cell cycle arrest at the G1 or G2/M
TumCCA↑,
BioAv↓, Experimental studies indicate that the oral absorption of kaempferol is relatively limited, with estimated intestinal absorption ranging between approximately 2% and 20%, depending on the administered form, food matrix, and experimental model
eff↑, kaempferol significantly enhances TRAIL-induced apoptosis in SW480 colon cancer cells through upregulation of DR4 and DR5.
DR4↑,
DR5↑,
Casp3↑, activation of caspases-9, -3, and -7.
Casp9↑,
Casp7↑,
TumCP↓, kaempferol inhibited proliferation and invasion while inducing both apoptosis and autophagy.
TumCI↓,
TumAuto↑,
mtDam↑, mitochondrial dysfunction, ROS generation, activation of p53 and MAPK signaling,
P53↑,
MAPK↑,
*lipid-P↓, Kaempferol significantly reduced lipid peroxidation in liver and blood tissues and restored antioxidant enzyme activities, including catalase, superoxide dismutase, and glutathione peroxidase.
*TAC↑,
*Catalase↑,
*SOD↑,
*GPx↑,
*NRF2↑, kaempferol multifaceted antioxidant actions—especially through Nrf2 activation, suppression of lipid peroxidation, and enhancement of endogenous enzyme defense
*Inflam↓, Lico A mitigates LPS-induced effects by inhibiting inflammatory cytokine production and NO through NF-κB pathway suppression.
*NO↓,
*NF-kB↓,
*TAC↑, Lico A enhances the activity of antioxidant enzymes and protects against oxidative damage and cell death via ERK and Akt pathways
Apoptosis?, Lico A exhibits significant anti-tumor effects (Kang et al., 2017; Wu et al., 2017; Chen et al., 2018a), including the induction of apoptosis in cancer cells, regulation of the cell cycle, inhibition of tumor invasion and metastasis, and suppression
TumCCA↑,
TumCI↓,
TumMeta↓,
TumCP↓,
MAPK↓, Lico A acts to inhibit this process by restraining cell migration, modulating E-cadherin and vimentin expression, and blocking MAPK and AKT signaling pathways (
Akt↓,
IL6↓, suppressing angiogenesis factors such as IL-6, IL-8, and the VEGFR-2 signaling pathway
IL8↓,
VEGFR2/KDR/Flk1↓,
LC3II↑, MCF-7 20–100 Activate the LC3-II signaling pathway while suppressing the PI3K/Akt/mTOR/signaling pathway
PI3K↓,
mTOR↓,
mtDam↑, Lymphoma T24 20–80 Induce mitochondrial dysfunction, decreased mitochondrial membrane potential
MMP↓,
*NRF2↑, Research has uncovered that Lico A’s anti-arthritis effects depend on the activation of the Keap1-Nrf2 signaling pathway through p62 phosphorylation at the Ser349 site
*PGE2↓, Skin inflammation HT1080/HDF post-shave irritation model Decreased NF-κB and PGE2 secretion
*Obesity↓, Research has shown that Lico A treatment in high-fat diet (HFD)-induced obese mice reduces body weight and decreases inguinal and epididymal adipose tissue compared to HFD-treated mice.
*SIRT1↑, Lico A’s specific lipid-lowering mechanism involves activating the SIRT1/AMPK pathway, reducing fatty acid synthesis, and enhancing lipolysis and beta-oxidation in hepatocytes
*AMPK↑,
*AntiFungal↑, Lico A exhibits substantial antifungal activity against Candida albicans, inhibiting biofilm formation by 35%–60%, and suppressing yeast-hyphal transformation and protease secretion
*AntiP↑, Additionally, Lico A reduces the total number of Schistosoma mansoni eggs, likely by increasing ROS production and inducing the death of adult Schistosoma mansoni
*BMD↑, Lico A administration restores or protects bone mass in disease states
*GastroP↑, ico A could promote intestinal epithelial renewal to exert intestinal protective effect
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IronCh↑, Lactoferrin (LF), a glycoprotein with strong iron chelating properties, can regulate its availability to cancer cells, thereby limiting their growth and progression.
ROS↓, By chelating free Fe ions, LF reduces oxidative stress and inhibits the mechanisms that promote carcinogenesis.
Imm↑, Additionally, it exhibits immunomodulatory and anti-inflammatory effects and may enhance the body’s anti-tumor response.
Inflam↓,
*BBB↑, LF crosses from the blood into the cerebrospinal fluid through the blood–brain barrier [25], where its beneficial effects have been documented in the context of neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, and de
Iron↝, Among the many biological properties of lactoferrin, its ability to strongly bind and transport iron ions over a wide range of pH values is a key function, determining its effectiveness in regulating iron homeostasis
*Fenton↓, LF, due to its ability to chelate iron, reduces its availability for the Fenton reaction, which reduces oxidative stress
*ROS↓,
*TAC↑, antioxidant properties of LF supplementation resulted in an increase in hydrophilic antioxidant capacity [151], a decrease in oxidative stress markers [152,153], and an increase in total antioxidant status (TAS)
*SOD↑, It also improved the levels of antioxidant markers, such as SOD, GPx, and glutathione, compared with the placebo group
*GPx↑,
*GSH↑,
*TBARS↓, Supplementation with LF-containing colostrum led to lower levels of thiobarbituric acid reactive substances (TBARS).
*PTEN↓, In addition, in patients with Alzheimer’s disease, LF supplementation led to the decreased expression of phosphatase and tensin homolog (PTEN), tau, and mitogen-activated protein kinase (MAPK1), as well as decreased serum levels of Aβ42, which ma
*tau↓,
*MAPK↓,
*Aβ42↓,
*Apoptosis↓, Reducing hydrogen peroxide-induced apoptosis through the inhibition of caspase-3 and Akt activation
*Casp3↓,
*Akt↑,
*GutMicro↑, LF shows a beneficial effect on the composition of the microbiota, promoting the growth of beneficial bacteria such as Bifidobacterium and Lactobacillus, while inhibiting the growth of pathogens such as Escherichia coli, Salmonella, and Shigella.
*Sepsis↓, A meta-analysis suggests that it may reduce the risk of fungal sepsis and shorten the hospitalization of preterm infants
*anemia↓, LF administration is a promising therapy for iron deficiency (ID) conditions, including iron deficiency anemia (IDA), both as a primary treatment and as an adjunctive therapy.
*IL6↓, ability to inhibit interleukin-6 (IL-6) expression, LF decreases hepcidin synthesis, which in turn increases ferroportin levels, restoring iron export from cells to the blood i
*FPN↑,
*TfR1/CD71↑, In addition, LF induces an increase in transferrin receptor 1 (TfR1) levels and a decrease in ferritin (Ftn) levels
*Ferritin↓,
*HemoG↑, Numerous intervention studies have confirmed the efficacy of LF supplementation, showing an increase in hemoglobin (Hb), total iron, erythrocyte count (RBC), and serum ferritin levels.
*RBC↑,
*eff↑, Most studies have shown similar or superior efficacy of bLF to traditionally used therapy (ferrous sulfate and ferric hydroxide) in restoring iron deficiency, with significantly fewer gastrointestinal side effects
*BioAv↓, Orally administered LF has low bioavailability due to degradation at unfavorable gastric pH and by proteolytic enzymes in the intestinal lumen and poor permeability through the intestinal epithelium, which limits its effective delivery to target site
*BioAv↑, LF is much better absorbed when administered directly into the duodenum. Therefore, ... coating enteral capsules containing LF, encapsulating it in nanocarriers, which allows it to be released at a site with less gastric pepsin activity
*BioAv↝, Other routes of administration, including transdermal or inhalation, are also being considered, which could avoid degradation in the gastrointestinal tract.
*ChemoSen↑, studies suggest that LF may act synergistically with other therapies such as chemotherapy, immunotherapy, and targeted therapy
*BioAv↑, Additionally, the use of probiotic bacteria as internal producers of LF in the body may open new perspectives for its therapeutic use.
Ferroptosis↑, LF also induces ferroptosis—iron-dependent cell death, which leads to excessive lipid oxidation in cell membranes and the destruction of cancer cells.
*Ach↑, AD patients showed decreased serum (ACh), (5-HT), antioxidant and anti-inflammatory markers, and decreased expression of Akt.., as well as PI3K, and p-Akt levels in PBL lysate; all these parameters were significantly improved after daily LF administr
*5HT↑,
*TAC↑,
*Inflam↓,
*Akt↑,
*PI3K↑,
*Aβ42↓, elevated serum amyloid β (Aβ) 42, cholesterol, oxidative stress markers, IL-6, heat shock protein (HSP) 90, caspase-3, and p-tau, as well as increased expression of tau, MAPK1 and PTEN in AD patients, were significantly reduced upon LF intake.
*LDL↓,
*ROS↓,
*IL6↓,
*HSP90↓,
*Casp3↓,
*tau↓,
*MAPK↓,
*PTEN↓,
*cognitive↑, reflected in enhanced cognitive function assessed by the Mini-Mental State Examination (MMSE) and Alzheimer's Disease Assessment Scale-Cognitive Subscale 11-item (ADAS-COG 11) questionnaires as clinical endpoints.
*Dose↝, received either standard therapy (group 1, AD patients without LF) or LF capsules (Jarrow Formulas®, USA, 250 mg/day, p.o.; group 2) [26] for three months.
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*antiOx↑, the antioxidant effect of lycopene
*ROS↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*BioAv↝, human body cannot synthesize lycopene. It must be supplied with the diet
*Half-Life↑, half-life of lycopene in human plasma is 12–33 days
*BioAv↓, bioavailability decreases with age and in the case of certain diseases
*BioAv↑, heat treatment process of food increases the bioavailability of lycopene
*cardioP↑, positive effect on cardiovascular diseases, including the regulation of blood lipid levels
*neuroP↑, beneficial effects in nervous system disorders, including neurodegenerative diseases such as Parkinson′s disease and Alzheimer′s disease
*H2O2↓, Lycopene has the ability to reduce reactive oxygen species (ROS) and eliminate singlet oxygen, nitrogen dioxide, hydroxyl radicals, and hydrogen peroxide
*VitC↑, ability to regenerate non-enzymatic antioxidants such as vitamin C and E.
*VitE↑,
*GPx↑, increase in cardiac GSH-Px activity and an increase in cardiac GSH levels
*GSH↑,
*MPO↓, also a decrease in the level of cardiac myeloperoxidase (MPO), cardiac H2O2, and a decrease in cardiac glutathione S transferase (GSH-ST) activity.
*GSTs↓,
*SOD↑, increasing the activity of GSH-Px and SOD in the liver
*NF-kB↓, reducing the expression of NF-κB mRNA in the heart
*IL1β↓, decreased the level of IL-1β and IL-6 and increased the level of anti-inflammatory IL-10 in the heart
*IL6↓,
*IL10↑,
*MAPK↓, inhibited the activation of the ROS-dependent pro-hypertrophic mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) signaling pathways.
*Akt↓,
*COX2/PTGS2↓, decrease in the levels of pro-inflammatory mediators in heart: COX-2, TNF-α, IL-6, and IL-1β and an increase in the anti-inflammatory cardiac TGF-β1.
*TNF-α↓,
*TGF-β1↑,
*NO↓, reduced NO levels in heart and cardiac NOS activity
*GSR↑, increase in the level of cardiac and hepatic SOD, CAT, GSH, GPx, and glutathione reductase (GR)
*NRF2↑, It also activated nuclear factor-erythroid 2 related factor 2 (Nrf2). This affected the downstream expression of HO-1 [97].
*HO-1↑,
*TAC↑, Researchers observed an increase in the liver in TAC and GSH levels and an increase in GSH-Px and SOD activity
*Inflam↓, study showed that lycopene was anti-inflammatory
*BBB↑, Lycopene is a lipophilic compound, which makes it easier to penetrate the blood–brain barrier.
*neuroP↑, Lycopene had also a neuroprotective effect by restoring the balance of the NF-κB/Nrf2 pathway.
*memory↑, lycopene on LPS-induced neuroinflammation and oxidative stress in C57BL/6J mice. The tested carotenoid prevented memory loss
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*antiOx↑, Anti‐oxidative mechanism of lycopene
*ROS↓, Lycopene inhibits ROS generation and subsequent oxidative stress by inducing antioxidant enzymes (SOD, CAT, GSH, GSH‐Px, and GST) and limiting MDA level and lipid peroxidation (LPO).
*SOD↑,
*Catalase↑,
*GSH↑,
*GSTs↑,
*MDA↓,
*lipid-P↓,
*NRF2↑, Lycopene also prevents ROS release by upregulating Nrf2‐mediated HO‐1 levels and inhibiting iNOS‐activated NO generation
*HO-1↑,
*iNOS↓,
*NO↓,
*TAC↑, upregulating total antioxidant capacity (TAC) and direct inhibition of 8‐OHdG, NOX4.
*NOX4↓,
*Inflam↓, Anti‐inflammatory mechanism of lycopene.
*IL1↓, IL‐1, IL‐6, IL‐8, IL‐1β, and TNF‐α release.
*IL6↓,
*IL8↓,
*IL1β↓,
*TNF-α↓,
*TLR2↓, prevents inflammation by inhibiting toll‐like receptors TLR2 and TLR4 and endothelial adhesion molecules VCAM1 and ICAM‐1.
*TLR4↓,
*VCAM-1↓,
*ICAM-1↓,
*STAT3↓, inhibiting STAT3, NF‐κB, ERK pathway, and IL‐6 and TNF‐α release.
*NF-kB↓,
*ERK↓,
*BP↓, Another clinical study demonstrated that consumption of raw tomato (200 g/day) could prevent type 2 diabetes‐associated cardiovascular diseases by lowering systolic and diastolic blood pressure, upregulating ApoA1, and downregulating ApoB levels
ROS↓, lycopene suppresses the metastasis of the SK‐HEP‐1 cell line by NOX‐4 mRNA expression inhibition and the reactive ROS intracellular activity inhibition
PGE2↓, Lycopene is also used to treat colorectal cancer cells in humans, and the introduction of lycopene decreases the prostaglandin E2 and nitric oxide levels
cardioP↑, Lycopene‐rich foods can be highly beneficial in preventing cardiovascular diseases as lycopene is a potential source of antioxidants
*neuroP↑, beneficial role of lycopene on aging‐related neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease, has been confirmed in both experimental and clinical trials
*creat↓, Several pre‐clinical studies reported that lycopene treatment significantly reduced serum urea and serum creatinine, as well as reversed various toxic chemical‐induced nephrotoxicity and oxidative damage by exhibiting excellent antioxidative properti
*RenoP↑,
*CRM↑, its potency in treating aging disorders and its role as a mimic of caloric restriction.
*AntiDiabetic↑, Metformin is a drug commonly prescribed to treat patients with type 2 diabetes.
*AntiAge↑, Here we show that long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice
*toxicity⇅, while a higher dose (1% w/w) was toxic.
*CRM↑, The effects of metformin resembled to some extent the effects of caloric restriction, even though food intake was increased.
*Strength↑, Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced LDL and cholesterol levels without a decrease in caloric intake
*LDL↓,
*AMPK↑, metformin increases AMP-activated protein kinase activity and increases antioxidant protection, resulting in reductions in both oxidative damage accumulation and chronic inflammation
*TAC↑,
*ROS↓, consistent with decreased oxidative stress damage in the liver of metformin-treated mice
*Inflam↓, Metformin inhibits chronic inflammation
Risk↓, metformin treatment has been associated with reduced risk of cancer4 and cardiovascular disease
*cardioP↑,
*ALAT↓, Ala aminotransferase (U/L) 90 ± 58 64 ± 29
*NRF2↑, The increase in Nrf2/ARE reporter activity occurred with an ED50 of ~1.5 mM metformin without reduction in cell survival
*SOD2↑, 0.1% metformin contributed to an increase in the level of antioxidant and stress response proteins, including SOD2, TrxR1, NQO1 and NQO2
*TrxR1↑,
*NQO1↑,
*NQO2↑,
*SOD↑, RFM can reduce oxidative stress, as evidenced by higher SOD and CAT activities in the CG than in samples placed in the RFM.
*Catalase↑,
*ROMO1↑, required 3hrs
*MDA↓, Too long a stay in the RMF at the frequency of 50 Hz increased the level
*TAC↑, RFM at 50 Hz increased the TAC level,
*ROS↓, In the case of ROMO1, it is stated that 1 h 25 Hz are the optimal conditions for no increased production of ROS.
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*memory↑, piperine improved the memory performance and myelin repair in the hippocampal demyelination model
*iNOS↓, Piperine inhibited iNOS expression concomitant with enhanced expression levels of Nrf2, HO1 and the total antioxidant capacity in the hippocampal tissue.
*NRF2↑,
*HO-1↑,
*TAC↑,
*TNF-α↓, Piperine treatment significantly reduced the gene expression level of TNF-α, IL1-β, NF-κB, and glial activation in the injured area;
*IL1β↓,
*NF-kB↓,
*IL10↑, however, the mRNA level of IL-10, Foxp3, BDNF and MBP were significantly increased
*FOXP3↑,
*BDNF↑,
other↑, piperine as a promising therapeutic target in MS patients
*Sepsis↓, results showed that quercetin reduced the tissue edema, congestion, and hemorrhage, increased the alveolar volume, and helped to maintain the lung anatomy of septic rats.
*ROS↓, Admistration of quercetin at the dosage of 15 and 20 mg/kg to septic rats caused significant reduction in the ROS levels.
*SOD↑, The results showed that administration of quercetin
at the dosage of 15 and 5 mg/kg to septic rats caused a significant increase in SOD, CAT, and APX expression levels
*Catalase↑,
*HMGB1↓, quercetin caused a significant decrease in HMGB1 protein levels
*Inflam↓, quercetin was found to reduce
the inflammation associated with sepsis
*TAC↑, significant increase in the expression of antioxidant
enzymes.
ROS↑, QH decreased the production of reactive oxygen species (ROS) and increased antioxidant capacity in PC3 cells at various concentrations (2.5‑60 µg/ml) with peak inhibition and augmentation changes of 3.22‑ and 3.00‑fold, respectively.
cl‑Casp3↑, activated/cleaved caspase-3 levels were found to be elevated at low concentration of QH (5 and 10 μg/ml) by ~1.5-fold and at higher concentrations (20 and 40 μg/ml) by ~2.7-fold (Fig. 2E). Poly(adenosine diphosphate ribose)
cl‑PARP↑, analysis revealed an increase in PARP cleavage in PC3 cells following QH treatment
miR-21↓, dose-dependent decrease in miR-21 expression, with inhibition rates of 42, 56 and 77% observed at 5, 10 and 20 μg/ml QH, respectively
PDCD4↑,
TAC↑,
tumCV↓, QH inhibits PC3 cell viability.
TumCI↓, QH inhibits the invasive activity of PC3 cells.
*Dose↝, Res functional selenium nanoparticles (Res@SeNPs) (8 ± 0.34 nm) were prepared first, after which the surface of Res@SeNPs was decorated with a blood-brain barrier transport peptide (TGN peptide) to generate Res-selenium-peptide nanocomposites (TGN-Re
*cognitive↑, Due to high BBB transport efficiency and regulatory effects on gut microbiota, TGN-Res@SeNPs is
superior to Res@SeNPs and Res in improving cognitive ability in vivo.
*Aβ↓, Oral administration of TGN-Res@SeNPs improves cognitive disorder through (1) interacting with Aβ and decreasing Aβ aggregation, effectively inhibiting Aβ deposition in the hippocampus;
*ROS↓, (2) decreasing Aβ-induced reactive oxygen species (ROS) and increasing activity of antioxidation enzymes in PC12 cells and in vivo;
*TAC↑,
*GutMicro↑, 4) alleviating gut microbiota disorder, particularly with respect to oxidative stress and inflammatory-related bacteria such as Alistipes, Helicobacter, Rikenella, Desulfovibrio, and Faecalibaculum.
*BBB↑, Res@SeNPs and TGN-Res@SeNPs had a higher BBB transport efficiency than Res.
Casp3↑, RQ also induced caspase-3-cleavage (2-fold) and increased PARP cleavage.
PARP↑,
survivin↓, RQ also decreased expression of survivin protein
miR-27a-3p↓, RQ decreased microRNA-27a (miR-27a) and induced zinc finger protein ZBTB10
Sp1/3/4↓, RQ treatment decreased the expression of Sp1, Sp3, and Sp4 mRNA and this was accompanied by decreased protein expression
ZBTB10↑,
ROS⇅, RQ slightly induced the generation of ROS at low concentrations (0–10 μg/mL) whereas at concentrations higher than 20 μg/mL generation of ROS was significantly reduced
TAC↑, RQ decreased the generation of reactive oxygen species (ROS) by up to 2.25-fold and increased the antioxidant capacity by up to 3-fold in HT-29 cells (3.8-60 μg/mL)
tumCV↓, HT-29 cell viability (Fig. 2A) was significantly decreased by RQ in a dose- and time-dependent manner
*antiOx↑, Rats in Group 4 (cadmium-exposed and Rosmarinic acid-accessed) exhibited increased levels of total proteins, a significant increase in the levels of antioxidant markers including total thiols, glutathione, total antioxidant capacity (TAC),
*Thiols↑,
*GSH↑,
*TAC↑, decreased levels of total thiols, GSH, catalase, and TAC
*SOD↑, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase, and a significant decrease in the levels of blood cadmium, ALP, ALT, AST, creatinine, blood urea nitrogen (BUN), urea, bilirubin, and oxidation markers (H2O2, and MDA
*GPx↑,
*Catalase↑,
*ALP↓,
*ALAT↓,
*AST↓,
*creat↓,
*BUN↓,
*H2O2↓,
*MDA↓,
*ROS↓, significantly help attenuate the oxidative stress induced by cadmium
cardioP↑, benefits of RA are attributed to its anti-cancer, anti-depressive, antiallergic, anti-inflammatory, anti-angiogenic, cardioprotective, hepatoprotective, nephroprotective, neuroprotective, antimicrobial, hypoglycemic, and hypolipidemic bioactivities
hepatoP↑,
neuroP↑,
*TAC↑, However, Se markedly attenuated AgNP-induced biochemical alterations, levels of TAC, CRP, and serum transaminases (AST, ALT) (P<0.05).
*CRP↓,
*AST↓, Pretreatment of rats with Se in AgNP-treated group caused reduction in the levels of AST and ALT
*ALAT↓,
*toxicity↓, Taken together, these findings suggest that administration of AgNPs produces hepatotoxicity in rats, whereas Se supplementation attenuates these effects.
*GSH↑, AgNPs’ treatment led to a decrease in the activity of GSH level, as shown in Figure 3A. However, pretreatment with Se (group 4) led to an increase in the levels of GSH
*SOD↑, Se pretreatment (group 4) increased the activities of SOD, CAT, and GSH-Px significantly (P<0.05) compared to the AgNP group.
*Catalase↑,
*hepatoP↑,
*NO↓, SMN lowered the H/R-elevated NO, MDA and carbonylated protein levels, while it enhanced the TAC level.
*MDA↓,
*TAC↑,
*Hif1a↓, SMN regulated the H/R up-regulated level of HIF-1α and iNOS in examined tissues.
*iNOS↓,
*ROS↓, Silymarin (200 mg/kg) treatment 30 mins post ICH injury prevented increase in oxidative stress markers and up-regulated antioxidant status.
*TAC↑,
*NF-kB↓, Silymarin treatment significantly down regulated the inflammatory responses by suppressing NF-κB-p65 levels and inflammasome-mediated caspase-1/IL-1β expressions.
*IL2↓,
*NRF2↑, treatment with silymarin post ICH injury increased Nrf-2/HO-1 and thereby improved overall cytoprotection.
*HO-1↑,
*neuroP↑, silymarin acts as neuroprotective compound by preventing inflammatory activation and up regulating Nrf-2/HO-1 signaling post ICH injury.
*Inflam↓,
*NLRP3↓, The NLRP3 mediated inflammatory responses were down regulated during silymarin treatment post ICH injury compared to ICH group
*RenoP↑, Shikonin significantly and dose-dependently alleviated gentamicin-induced renal injury, as revealed by restoring normal kidney function and histological architecture.
*ROS↓, Shikonin Defended against Renal Oxidative Stress and Activated the SIRT1/Nrf2/HO-1 Cascades in Rats with Gentamicin-Induced Renal Damage
*SIRT1↓,
*NRF2↑,
*HO-1↑,
*GSH↑, significant rise in GSH, TAC levels, and SOD activity, as well as SIRT1, Nrf2, and HO-1 protein levels
*TAC↑,
*SOD↑,
*MDA↓, significant decrease in the renal MDA, NO, and iNOS
*NO↓,
*iNOS↓,
*NHE3↑, shikonin treatment significantly and dose-dependently enhanced the reduced NHE3 level and mRNA expression induced by repeated gentamicin injections,
*PI3K↑, in the current study, shikonin treatment of the gentamicin-injected groups increased PI3K
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*ROS↓, we showed that Terminalia bellirica (Gaertn.) Roxb. extract (TBE) inhibits inflammatory response and reactive oxygen species (ROS) production in THP-1 macrophages.
*MAPK↓, TBE and GA attenuated LPS-induced inflammatory mediator expression, ROS production, and activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) in RAW 264 macrophages.
*NF-kB↓,
*TAC↑, TBE and GA increased antioxidant enzyme expression along with upstream mediators nuclear factor erythroid-2-related factor 2 (Nrf2), Akt, and AMP-activated protein kinase (AMPK).
*NRF2↑,
*Akt↑,
*AMPK↑,
*Inflam↓, In conclusion, TBE and GA exert protective effects against inflammation and oxidative stress by suppressing MAPK/NF-κB pathway and by activating Akt/AMPK/Nrf2 pathway.
*antiOx↑, All the extracts indicated antioxidant activity reflected through significant DPPH, TPC, FRAP, and beta carotene as‐69.13 ± 3.00, 1148.92 ± 14.01, 752.44 ± 10.30, and 65.74 ± 3.28, respectively.
*TOS↑, improvement in sensorimotor function restoration, muscle mass restoration, a substantial decrease in TOS, a significant increase in TAC, and enhanced antioxidative enzyme activity.
*TAC↑,
*neuroP↑, isolation of theaflavin from black tea and probed for their neuroprotective effect in mice model
*cognitive↑, TQ significantly improved cognition
*SOD↑, TQ significantly increased SOD and TAC and decreased AChE activities.
*TAC↑,
*AChE↓,
*MDA↓, It also decreased MDA and NO levels as well as TNF-α immunoreactivity and increased BDNF and Bcl-2 levels as well as ACh immunoreactivity.
*NO↓,
*TNF-α↓,
*Bcl-2↑,
*Ach↑,
*neuroP↑, These results indicate that TQ holds potential for neuroprotection and may be a promising approach for the treatment of neurodegenerative disorders.
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Review, |
Stroke, |
NA |
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*BioAv↓, TQ has poor bioavailability and is hydrophobic, prohibiting clinical trials with TQ alone.
*BioAv↑, TQ nanoparticle formulation shows better bioavailability than free TQ,
*Inflam↓, anti-inflammatory effects of TQ involve multiple complex signaling pathways as well as molecular mechanisms
*antiOx↑, antioxidant activity from the inhibition of oxidative stress
*ROS↓,
*GSH↑, GSH prevented ROS-mediated oxidative stress damage
*GSTs↑, TQ was found to exhibit antioxidant properties by increasing the levels of GSH and glutathione-S-transferase enzyme alpha-3 (GSTA3)
*MPO↓, TQ significantly reduced the disease activity index (DAI) and myeloperoxidase (MPO) activity, protecting the internal microenvironment of the colon.
*NF-kB↓, TQ reduced NF-κB signaling gene expression while alleviating the increase of COX-2 in skin cells induced by 12-O-tetradecanoylphorbol-13-acetate
*COX2/PTGS2↓,
*IL1β↓, reduced the expression of inflammatory factors such as IL-1β, TNF-α, IFN-γ, and IL-6
*TNF-α↓,
*IFN-γ↓,
*IL6↓,
*cardioP↑, TQ may exhibit substantial effects in the control of inflammation in CVD
*lipid-P↓, TQ reduces lipid accumulation and enhances antioxidant capacity and renal function.
*TAC↑,
*RenoP↑,
Apoptosis↑, Breast cancer TQ induces apoptosis and cell cycle arrest; reduces cancer cell proliferation, colony formation, and migration;
TumCCA↑,
TumCP↓,
TumCMig↓,
angioG↓, Colorectal Cancer (CRC) TQ inhibits the angiogenesis
TNF-α↓, Lung cancer TQ inhibits tumor cell proliferation by causing lung cancer cell apoptosis to significantly arrest the S phase cell cycle and significantly reduce the activity of TNF-a and NF-κB
NF-kB↓,
ROS↑, Pancreatic cancer TQ significantly increases the level of ROS production in human pancreatic cancer cells
EMT↓, TQ initiates the miR-877-5p and PD-L1 signaling pathways, inhibiting the migration and EMT of bladder cancer cells.
*Aβ↓, TQ significantly reduced the expression of Aβ, phosphorylated-tau, and BACE-1 proteins.
*p‑tau↓,
*BACE/β-secretase↓,
*TLR2↓, Parkinson’s disease (PD) TQ inhibits activation of the NF-κB pathway.
TQ reduces the expression of TLR-2, TLR-4, MyD88, TNF-α, IL-1β, IFN-β, IRF-3, and NF-κB.
*TLR4↓,
*MyD88↓,
*IRF3↓,
*eff↑, TQ pretreatment produced a dose-dependent reduction in the MI area and significantly reduced the elevation of serum cardiac markers caused by ISO.
eff↑, Curcumin and TQ induced apoptosis and cell cycle arrest and reduced cancer cell proliferation, colony formation, and migration in breast cancer cells
DNAdam↑, nanomedicine with TQ that induced DNA damage and apoptosis, inhibited cell proliferation, and prevented cell cycle progression
*iNOS↓, TQ significantly reduced the expression of COX-2 and inducible nitric oxide synthase (iNOS)
*RenoP↑, Pre-, post-, and cotreatment with TQ alleviated kidney injury
*TAC↑, by replenishing antioxidant reserves, reducing serum toxicity, decreasing ROS generation and lipid peroxidation, downregulating p38 MAPK/NF-κB axis/pathway proteins, and upregulating Nrf2 and HO-1,
*ROS↓, high-dose TQ alleviated ROS and H2O2 levels in groups III and IV
*lipid-P↓,
*p38↓,
*MAPK↓,
*NF-kB↓,
*NRF2↑,
*HO-1↑,
*MDA↓, TQ diminishes MDA levels
*GPx↑, GPx, GR, and CAT : restoration of GSH reserves and the abovementioned antioxidant enzymes
*GSR↑,
*Catalase↑,
*BUN↓, noticeable inhibition was observed in BUN, Cr, LDH, and KIM-1 at both doses
*LDH↓,
*IL1β↓, downregulation of IL-1β, diminishing inflammation
*Inflam↓, anti-inflammation, anti-oxidation, anti-bacteria, anti-fungal, and anti-tumor potential
*antiOx↑,
*Bacteria↓,
AntiTum↑,
*toxicity∅, A high dose of thymol up to 500 mg/kg diet has been shown to have no toxicity
*IBI↑, thymol improves intestinal integrity and alleviates intestinal injury via the regulation of the immune response and oxidation-reduction homeostasis
*ZO-1↑, increasing the expression of the tight junction protein zonula occludens-1 (ZO-1) and occludins
*OCLN↑,
*COX1↑, up-regulates cyclooxygenase-1 (COX1) activity
*TLR4↓, thymol inhibits TLR4 expression and then inhibits the activation of NF-κB signaling, which reduces the production of inflammatory cytokines, such as TNF-α and IL-1β [58,59]
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*TAC↑, Thymol Improves Anti-Oxidant Capacity in IBD
*NRF2↑, Studies have indicated that thymol activates Nrf2 signaling in different tissues
*GutMicro↑, Thymol Changes Gut Microbes and Prevents Pathogen Infection. thymol also promoted the colonization of beneficial bacteria, such as Clostridium, Lactobacillus, and Bacteroides, to improve gut health
*Dose↝, Sco (2 mg/kg/day, i.p.), Sco + vitexin (30 mg/kg/day, oral), Sco + donepezil (1.5 mg/kg/day, i.p.), vitexin alone, and donepezil alone
*Learn↑, co significantly impaired spatial learning and memory while increasing anxiety-like behaviors. Vitexin treatment markedly improved these deficits, with efficacy comparable to donepezil
*memory↑,
*AChE↓, Sco elevated acetylcholinesterase activity, lipid peroxidation, and oxidative/nitrosative stress markers (TOS, OSI, MDA, Peroxynitrite, NO, and NOS) while decreasing total antioxidant status (TAS). Vitexin reversed these changes.
*lipid-P↓,
*TOS↓,
*MDA↓,
*ONOO↓,
*NO↓,
*NOS2↓,
*TAC↑,
*BDNF↑, Sco reduced hippocampal BDNF, GDNF, PSD95, and synaptophysin levels and increased GFAP, IL-6, TNF-α, NF-κB p65, and COX-2 expression. Vitexin restored neurotrophic and synaptic proteins, suppressed astrocyte activation and inflammatory signaling, a
*GDNF↑,
*PSD95↑,
*GFAP↓,
*NF-kB↓,
*COX2/PTGS2↓,
*NRF2↑, and activated the Nrf2/HO-1 pathway.
*HO-1↑,
*neuroP↑, vitexin exerts significant neuroprotective and synaptoprotective effects against Sco-induced cognitive impairment by simultaneously restoring redox balance
*NeuroI↓, suppressing neuroinflammation, and preserving synaptic integrity.
Showing Research Papers: 1 to 48 of 48
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 48
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, Iron↝, 1, Keap1↑, 1, MFN2↑, 1, ROS↓, 2, ROS↑, 5, ROS⇅, 1, TAC↑, 2, TrxR↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1, mtDam↑, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
PPARγ↝, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Akt↑, 1, Apoptosis?, 1, Apoptosis↑, 6, BAX↑, 1, Casp3↑, 4, cl‑Casp3↑, 2, cl‑Casp3⇅, 1, Casp7↑, 1, Casp9↑, 4, Cyt‑c↑, 2, DR4↑, 1, DR5↑, 1, Ferroptosis↑, 1, MAPK↓, 1, MAPK↑, 1, MAPK↝, 1, p38↑, 1, PDCD4↑, 1, PUMA↑, 1, survivin↓, 2,
Kinase & Signal Transduction(tgid=6) ⓘ
SOX9↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
miR-21↓, 1, miR-27a-3p↓, 1, other↑, 1, tumCV↓, 3,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3II↑, 1, TumAuto↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1, P53↑, 2, PARP↑, 1, cl‑PARP↑, 3,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↑, 1, TumCCA↑, 5,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, ERK↓, 1, FOXO3↑, 1, mTOR↓, 1, mTOR↝, 1, PI3K↓, 1, RUNX2↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
CC(CDKs/cyclins)↓, 1, TumCI↓, 6, TumCMig↓, 2, TumCP↓, 4, TumMeta↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, VEGFR2/KDR/Flk1↓, 1, ZBTB10↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 3, IL6↓, 2, IL8↓, 1, Imm↑, 2, Inflam↓, 2, NF-kB↓, 4, PD-L1↓, 1, PGE2↓, 1, TNF-α↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, ChemoSen↑, 4, Dose↝, 1, eff↓, 1, eff↑, 6, RadioS∅, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 2, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, AntiTum↑, 1, cardioP↑, 3, chemoP↑, 1, hepatoP↑, 1, neuroP↑, 1, radioP↑, 2, Risk↓, 2,
Total Targets: 92
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
anemia↓, 1, AntiArt↑, 1, AntiBio↑, 2, AntiP↑, 1, Aβ42↓, 2, Eos↓, 1, FPN↑, 1, GDNF↑, 1, GFAP↓, 1, IgE↓, 1, IL13↓, 1, Learn↑, 2, NeuroI↓, 1, NLR↓, 1, ONOO↓, 1, RBC↑, 1, TRPA1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, antiOx↑, 15, Catalase↓, 1, Catalase↑, 16, Copper↓, 1, Fenton↓, 1, Ferroptosis↓, 1, GPx↑, 13, GPx4↑, 1, GSH↑, 16, GSR↑, 2, GSTA1↑, 2, GSTs↓, 1, GSTs↑, 3, H2O2↓, 2, HO-1↓, 1, HO-1↑, 11, lipid-P↓, 10, MDA↓, 20, MPO↓, 2, NOX4↓, 1, NQO1↑, 4, NRF2↓, 1, NRF2↑, 19, ROMO1↑, 1, ROS↓, 32, SOD↓, 1, SOD↑, 21, SOD1↑, 1, SOD2↑, 1, TAC↑, 46, TBARS↓, 1, Thiols↑, 1, TOS↓, 1, TOS↑, 1, TrxR1↑, 1, VitC↑, 1, VitE↑, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
Ferritin↓, 1, TfR1/CD71↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 6, AMPK↑, 3, BUN↓, 2, cAMP↑, 1, CRM↑, 2, glucose↓, 1, GlucoseCon↑, 1, LDH↓, 2, LDH↑, 1, LDL↓, 2, NADPH↑, 1, PKM2↓, 1, PPARγ↓, 1, PPARγ↑, 1, SIRT1↓, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Akt↑, 3, Apoptosis↓, 4, BAX↓, 1, Bcl-2↑, 2, Casp3↓, 4, Cyt‑c↓, 1, Ferroptosis↓, 1, iNOS↓, 6, MAPK↓, 5, p38↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 2, other↑, 2,
Protein Folding & ER Stress(tgid=8) ⓘ
HSP90↓, 1, NQO2↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
ATG5↑, 1, Beclin-1/ATG6↑, 1, LC3B↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, GSK‐3β↓, 1, PI3K↓, 1, PI3K↑, 2, PTEN↓, 2, p‑PTEN↑, 1, STAT3↓, 1, TRPM7↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, APP↓, 1, LRP1↑, 1, MMP9↑, 1, PKCδ↑, 1, SMAD3↓, 1, TGF-β1↓, 1, TGF-β1↑, 1, TJ↑, 1, VCAM-1↓, 1, Vim↓, 1, ZO-1↑, 1, α-SMA↓, 1, β-catenin/ZEB1↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hif1a↓, 2, NO↓, 10,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 4, GastroP↑, 1, IBI↑, 2, NHE3↑, 1, OCLN↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↑, 1, COX2/PTGS2↓, 4, CRP↓, 2, FOXP3↑, 1, GM-CSF↓, 1, HMGB1↓, 1, ICAM-1↓, 1, IFN-γ↓, 1, IL1↓, 1, IL10↓, 1, IL10↑, 3, IL1β↓, 10, IL2↓, 1, IL4↓, 1, IL4↑, 1, IL5↓, 1, IL6↓, 9, IL8↓, 1, Imm↑, 1, Inflam↓, 22, Inflam↑, 1, MyD88↓, 1, NF-kB↓, 14, PGE2↓, 2, TLR2↓, 2, TLR4↓, 4, TNF-α↓, 12,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↑, 1, AChE↓, 4, BDNF↑, 4, PSD95↑, 1, tau↓, 4, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 7, BACE/β-secretase↓, 3, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 4, BioAv↑, 6, BioAv⇅, 1, BioAv↝, 3, ChemoSen↑, 1, Dose↑, 1, Dose↝, 7, eff↑, 9, Half-Life↑, 1, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 6, Albumin↑, 1, ALP↓, 1, AST↓, 5, BMD↑, 1, BP↓, 1, creat↓, 2, CRP↓, 2, Ferritin↓, 1, GutMicro↑, 5, HemoG↑, 1, IL6↓, 9, LDH↓, 2, LDH↑, 1, NOS2↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 3, cardioP↑, 7, chemoP↑, 1, cognitive↓, 1, cognitive↑, 7, hepatoP↑, 4, memory↑, 7, neuroP↑, 11, Obesity↓, 1, QoL↑, 1, radioP↑, 1, RenoP↑, 5, Strength↑, 1, toxicity↓, 3, toxicity⇅, 1, toxicity↝, 1, toxicity∅, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 2, AntiViral↑, 1, Bacteria↓, 2, IRF3↓, 1, Sepsis↓, 2,
Total Targets: 210
Scientific Paper Hit Count for: TAC, total antioxidant capacity
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
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