Wound Healing Cancer Research Results
Wound Healing, Wound Healing: Click to Expand ⟱
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Scientific Papers found: Click to Expand⟱
*Bacteria↓, strong antibacterial, anticancer, anti-inflammatory, and wound-healing properties.
AntiCan↑,
*Inflam↓,
*Wound Healing↑,
eff↑, Cytotoxic effects of anticancer drugs such as verapamil, cisplatin, carmustine, and methotrexate are improved by citrate-coated silver oxide NP
ChemoSen↑,
EGFR↓, silver (AgNPs), gold (AuNPs), and superparamagnetic iron oxide nanoparticles (SPIONPs) have shown the
ability to interfere with EGFR
ROS↑, In MCF-7 breast cancer cells, AgNP induced ROS activated proteins, such as p53, Bax, and caspase-3, cause programmed cell death
P53↑,
BAX↑,
Casp3↑,
toxicity↝, AgNPs produce ionic silver and ROS that have
antibacterial properties, but their non-specific absorption
can harm healthy cells.
Wound Healing↑, The notable antimicrobial properties of silver render it indispensable for wound healing, infection control, cancer therapy and tissue regeneration applications.
AntiCan↑,
other↑, Additionally, AgNPs hold great promise as versatile drug carriers for targeted therapies and as contrast agents for advanced medical imaging techniques
MPT↑, these nanoparticles exert their effects by disrupting cell membrane permeability, interfering with cellular respiration processes and instigating the production of free radicals.
ROS↑,
other↑, Additionally, it has been proposed that AgNPs may release silver ions, which can bind to thiol groups found in essential enzymes, rendering them inactive
DNAdam↑, DNA typically contains sulfur, and nanoparticles may interact with these bases, potentially causing damage to the DNA molecule, and thereby contributing to cell demise
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*Wound Healing↑, unique antimicrobial properties silver nanocrystallites have garnered substantial attention and are used extensively for biomedical applications as an additive to wound dressings, surgical instruments and bone substitute materials.
*eff↝, cytotoxicity was dependent on various factors such as surface charge and coating materials used in the synthesis, particle aggregation, and the cell-type for the different silver nanoparticles that were investigated.
*toxicity↝, uncoated or colloidal silver nanoparticles were found to be the least toxic to both macrophage and lung epithelial 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
*Wound Healing↑, Antimicrobial effect of AgNPs allows effective use in wound healing and dentistry
*AntiThr↑, AgNPs possess antithrombotic activity useful to treat cardiovascular diseases.
*AntiAg↑, Their anti-platelet effects can be attributed to their ability to prevent or inhibit platelets from adhering to each other.
eff↑, AgNPs makes them excellent agents for photothermal therapy in the treatment of tumours and cancers.
*Bacteria↓, Ch-AgNPs (8–48 nm) exhibited significant antibacterial and antibiofilm activity.
*Wound Healing↑, Ch-AgNPs promoted wound healing activity at 75 and 100 μg mL−1 after 24 h.
TumCG↓, Ch-AgNPs effective inhibited the MCF-7 human breast cancer cells at 100 μg mL−1 after 24 h.
*Bacteria↓, Further, the silver chitosan nanoparticles showed antibacterial activity against two important clinical pathogens, S. aureus and E. coli.
*Wound Healing↑, Chitosan and silver each address infection and wound healing through distinct mechanisms.
*Bacteria↓, Overall, these results highlight Ag-Chi-NPs as sustainable bio-nanocomposites that combine antioxidant, antibacterial, and cytocompatibility properties, making them promising candidates for wound healing materials, antimicrobial coatings
*Wound Healing↑,
*Bacteria↓, Chi/Ag-NPs showed promising antifungal features against Candida albicans, Aspergillus fumigatus, Aspergillus terreus, and Aspergillus niger, where inhibition zones were 22, 29, 20, and 17 mm, respectively.
*Wound Healing↑, Wound healing results illustrated that fibroblasts advanced toward the opening to close the scratch wound by roughly 50.5% after a 24-h exposure to Chi/Ag-NPs, greatly accelerating the wound healing process.
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*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].
*Inflam↓, anticancer, anti-edema, anti-inflammatory, anti-microbial, anti-coagulant, anti-osteoarthritis, anti-trauma pain, anti-diarrhea, wound repair.
*Bacteria↓,
*Pain↓,
*Diar↓,
*Wound Healing↑,
ERK↓, Figure 1
JNK↓,
XIAP↓,
HSP27↓,
β-catenin/ZEB1↓,
HO-1↓,
lipid-P↓,
ACSL4↑,
ROS↑,
SOD↑,
Catalase↓,
GSH↓,
MDA↓,
Casp3↓,
Casp9↑,
DNAdam↑,
Apoptosis↑,
NF-kB↓,
P53↑,
MAPK↓,
APAF1↑,
Cyt‑c↓,
CD44↓,
Imm↑, Bromelain was also studied in the innate immune system, where it could enhance and sustain the process
ATG5↑,
LC3I↑,
Beclin-1↑,
IL2↓, bromelain in vitro experiments resulted in diminished amounts of IL-2, IL-6, IL-4, G-CSF, Gm-CSF, IFN-γ,
IL4↓,
IFN-γ↓,
COX2↓, proprietary bromelain extract could decrease IL-8, COX-2, iNOS, and TNF-α without affecting cell viability.
iNOS↓,
ChemoSen↑, Bromelain may increase the cytotoxicity of cisplatin in the treatment of breast cancer as reported in 2 studies with MDA-MB-231 and 4T1 Breast Tumor cell lines
RadioS↑, The size and weight of tumors in gamma-irradiated EST-bearing mice treated with bromelain decreased significantly with a significant amelioration in the histopathological examination
Dose↝, oral bromelain administration in breast cancer patients (daily up to a dose of 7800 mg)
other↓, The role of bromelain (in combination with papain, sodium selenite and Lens culinaris lectin) has been also tested as a complementary medicine on more than 600 breast cancer patients to reduce the side effects caused by the administration of the adju
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*Risk↓, Arthritic bone is associated with almost a 20-fold decrease in boron content.
*eff↑, placebo-controlled supplementation trial conducted in Australia, in which a significantly favorable response to a supplement of 6 mg of boron per day (sodium tetraborate decahydrate) was seen in 20 subjects with OA
*SOD↑, Human studies of boron deprivation and repletion have shown that boron significantly increases erythrocyte superoxide dismutase (SOD) activity.
*NF-kB↓, There is evidence that Boron down-regulates inflammation through the NF-(kappa) B
pathway
*Risk↓, In areas where boron intake is usually 3 to 10 mg/d, estimated incidence of arthritis ranges from 0% to 10%.
*CRP↓, a significant increase in concentrations of plasma boron occurred 6 hours after supplementation with 11.6 mg of boron, coupled with significant decreases in levels of hs-CRP and TNF-α.
*TNF-α↓,
*Wound Healing↑, Mechanisms implicated in the effects of boron on wound healing / fibroblast control by boron
TumCMig↓, Both polyphenols induced migration inhibition, resulting in practically halting the wound closure.
Wound Healing↑,
eff↑, CAPE produced better results than CA with the same doses and experiment times
tumCV↓, In the case of CA treatment of MCF-7 cells (Figure 2A and D), cell viability decreased in a dose-dependent manner, falling from 93.5% for a dose of 10 µM, 83.1% for 25 µM,
*Bacteria↓, properties including anti-viral, anti-bacterial, anti-cancer, immunomodulatory, and wound-healing activities.
*AntiCan↑,
*Imm↑,
*Wound Healing↑,
*NF-kB↓, including inhibition of the transcription factors NF-κB
*5LO↓, use of CAPE in diabetes therapy have shown that caffeic acid phenethyl ester inhibits the enzyme 5-lipoxygenase
*AntiDiabetic↑, Antidiabetic Properties
ChemoSen↑, CAPE treatment enhances the antitumor effect of cytostatic drugs, such as vinblastine, paclitacol, estramustine and docetaxel, used in the chemotherapy of prostate cancer [76,81,82].
selectivity↑, CAPE acts selectively on diseased cells, without adversely affecting normal cells [88]
chemoPv↑, CAPE may be useful as support for cancer therapy in terms of chemoprevention of non-cancerous cells
*antiOx↑, including anti-oxidant, anti-inflammatory, antilipidemic, antidiabetic, and antihypertensive activities.
*Inflam↓,
*AntiDiabetic↑,
*Obesity↓, chlorogenic acid as a nutraceutical for the prevention and treatment of metabolic syndrome and associated disorders, including in vivo studies, clinical trials, and mechanisms of action
*Wound Healing↑, It was found that chlorogenic acid accelerated wound healing.
*BP↓, Significant reductions of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were observed
*Dose↝, A total of 23 healthy subjects (four men and 19 women) were given water (control) and 400 mg of chlorogenic acid dissolved in 200 mL of low nitrate water.
*ROS↓, the mechanism proposed was that chlorogenic acid scavenges reactive oxygen species (ROS) generated by consumption of high-fat diet, which suppresses the expression of inflammation, and consequently reduces fat accumulation,
*Fas↓, chlorogenic acid supplementation in high-fat diet-induced-obese mice significantly inhibited fatty acid synthase (FAS),
*HMG-CoA↓, As for hypercholesterolemia, chlorogenic acid has been found to inhibit 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR)
*GutMicro↑, high-CGAs coffee (80.8 mg) induced a significant increase in the growth of Bifidobacterium spp. as well as Clostridium coccoides-Eubacterium rectale group, the latter group having also potential to benefit human health.
DDS↑, ecent scientific research demonstrates that
chitosan represents a valuable candidate for designing non-invasive drug delivery strategies.
toxicity↓, Chitosan nanoparticles are capable of optimizing drug pharmacokinetics, increasing local drug
concentrations, and reducing overall systemic toxicity.
TJ↓, Its positively charged amino groups give it unique properties, including mucoadhesion, the ability to open epithelial tight junctions, and strong interactions with negativelycharged biological membranes, which helps increase the bioavailability of d
BioAv↑,
*Bacteria↓, Beyond its role in drug delivery, chitosan also has antimicrobial, antiinflammatory, antioxidant, and tissue-regenerating effects
*Inflam↓,
*antiOx↓,
Wound Healing↑, (used in wound healing
other↝, Chitosan nanoparticles are most commonly produced via ionotropic gelation, where positively
charged amino groups interact with multivalent anions, such as tripolyphosphate (TPP).
eff↑, Chitosan-based hydrogels can be adapted to respond to physiological stimuli, especially
changes in pH.
eff↑, acidic tumor microenvironments, pH-sensitive chitosan releases drugs, while under redox conditions with
elevated GSH levels, carriers disintegrate, ensuring intracellular drug delivery
other↝, A common method for the synthesis of chitosan is the deacetylation of chitin using sodium hydroxide in excess as a reagent and water as a solvent
other↝, molecular weight of chitosan is between 3800 and 20,000 Daltons. The degree of deacetylation (%DD) ranges from 60% to 100%.
*Weight↝, chitosan and fat is not very well understood and has not been proved clinically yet, chitosan has been used as an effective complement to help lose weight during diet period or to stabilise one's weight
*toxicity↓, Since they are biocompatible, biodegradable, mucoadhesive, and nontoxic, with antimicrobial, antiviral, and adjuvant properties, chitin and chitosan have been widely applied in medicine and pharmacy
*Bacteria↓,
*BioAv↑,
DDS↑, Combined with drugs such as doxorubicin, paclitaxel, docetaxel, and norcantharidin, chitin and chitosan are used as drug carriers.
*Wound Healing↑, Moreover, chitin has some unusual properties that accelerate healing of wounds in humans
*other↝, Because of its mucoadhesive properties, chitin and chitosan are widely applied for mucosal routes of administration, that is, oral, nasal, and ocular mucosa, which are noninvasive routes.
*Imm↑, hypothesized that a viscous chitosan solution, when administered subcutaneously, would not only provide immune stimulation as previously
eff↑, With the development of nanotechnology, chitosan have shown its unique advantages when combined with nanoparticles.
*BioAv↝, Chitosan is soluble in diluted acids but is relatively insoluble in water [66, 67]. The poor solubility of chitosan poses limitations for its biomedical applications.
*BioAv↑, By attaching galactose molecules to the chitosan molecules, a new water-soluble compound, glycated chitosan (GC), was formed
eff↑, Chitosan nanoparticles (CNPs) can be administrated through noninvasive routes such as oral, nasal, pulmonary, and ocular routes
NK cell↑, CNP remarkably increased the killing activities of NK cells activity
IL2↑, CNP also significantly promoted the production of Th1 (IL-2 and IFN-γ) and Th2 (IL-10) cytokines
IFN-γ↑,
IL10↑,
DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)
Wound Healing↑, possible mechanisms of how chitosan enhances coagulation and wound healing are also discussed.
Imm↑, demonstrate immune and antitumor effects are also discussed
AntiTum↑,
AGEs↓, Chitosan that can help reduce AGE (advanced glycation endproducts) levels in patients with prostate cancer.
Wound Healing↑, Chitosan is approved by the FDA for use in wound dressings
Obesity↓, been used in published clinical trials for weight loss but is not approved for the purposes of this study.
BioAv↑, attractive properties such as solubility in acidic aqueous media, reactive functional groups for functionalization and crosslinking [ 11 ], non-oxidation, biodegradability, muco adhesibility, biocompatibility, and FDA approval for use in wound dressi
Wound Healing↑,
DDS↑, The most important properties that chitosan provides when included in drug delivery systems is the protection of the physiological environment [ 30 ], increases bioavailability, is biocompatible, so it will not generate toxicity
toxicity↓,
eff↑, In the development of new delivery systems based on chitosan and other materials, it is possible to think about the inclusion of several drugs and the synergy of the materials, to improve the therapy and to continue avoiding the unpleasant side effec
DDS↑, attained promising recognition from researchers for improving the pharmacokinetics and pharmacodynamics of chemotherapeutics.
eff↓, CS-NPs for target-specific delivery of chemotherapeutics have also been considered.
*Bacteria↓, Owing to their inherent antimicrobial, antioxidant, wound healing, analgesic, anti-rheumatic, immunomodulatory, mucoadhesive, antiproliferative, and antimetastatic properties, CS and CS-NPs have been extensively investigated
*antiOx↑,
*Wound Healing↑,
*Imm↑,
TumCP↓,
TumMeta↓,
angioG↓, anticancer potential of CS and CS-NPs was attributed to their antiangiogenic, antioxidant, immunoenhancing, and apoptotic effects
Apoptosis↑,
ROS↑, apoptotic effect of CS-NPs is due to the generation of reactive oxygen species (ROS), which induce apoptosis and cause severe stress to the mitochondria and endoplasmic reticulum.
ER Stress↑,
BioAv↑, CS-NPs improve the rate and extent of absorption of chemotherapeutics from the site of administration owing to their prolonged residence time.
Half-Life↑,
eff↑, interesting approach employing high-intensity ultrasound was proposed by Choi et al35 to improve the penetration of CS-NPs into tumor tissues.
EPR↑, permeated CS-NPs were retained in tumor tissues for longer periods. This phenomenon is called “Enhanced Permeation and Retention (EPR)” effect.
ChemoSen↑, In addition to monodelivery, CS-NPs have shown tremendous potential for combined delivery of chemotherapeutics.
eff↑, CS-NPs have been conjugated with a variety of targeting ligands (eg, folic acid, hyaluronic acid, transferrin, antibodies, peptides, and aptamers) to enable selective intracellular delivery.
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*neuroP↑, This versatile spice has shown potential as a natural remedy fora wide range of chronic diseases, such as neurodegenerative disorders, type 2 diabetes,cardiovascular problems, and metabolic sy
*AntiDiabetic↑,
*tau↓, Key compounds in cinnamon, particularly cinnamaldehyde, are believed to protect the brain by inhibiting the aggregation of tau and amyloid-beta (Aβ) proteins, both of which are hallmark features of Alzheimer’s disease.
*Aβ↓,
*antiOx↑, cinnamon’s antioxidant and anti-inflammatory properties help mitigate oxidative stress and inflammation in the brain
*Inflam↓,
*ROS↓, Neurochemicalanalysis showed reduced oxidative stress, evidenced by lower levels of malondialdehyde and nitrites, as well as increased reduced glutathione.
*MDA↓,
*GSH↓,
*cardioP↑, es, has long beenutilized in herbal medicine to support cardiovascular health and treat cardiovascular diseases(CVDs
*LDL↓, Specifically, cinnamon can lower levels of LDL (bad) cholesterol andtriglycerides, while increasing HDL (good) cholester
*HDL↑,
*other↝, particularly beneficial for treatinginflammatory bowel diseases (IBD) such as colitis.
*TNF-α↓, lowering levels of inflammatory markers such as TNF-α, IL-6, and MPO, andby downregulating the expression of TLR-4.
*IL6↓,
*MPO↓,
*TLR4↓,
*GutMicro↑, cinnamon can also support a balanced gut microbiota, which is essential for overall digestive health. By inhibiting the growth of harmful bacteria and fungi, while promoting the growth of beneficial microorganisms
*lipid-P↓, can improve ulcerative colitis (UC) in rats by reducinginflammation, lipid peroxidation, and histological damage
*Wound Healing↑, Combining cinnamon oil(CO) with aloe vera (AV) (COVA) has been shown to effectively inhibit bacterial growth and promote wound healing.
*antiOx↑, contains various chemical compounds demonstrate significant antioxidant properties including caffeic acid, myricetin, rutin, quercetin, α-tocopherol, papain, benzyl isothiocyanate (BiTC), and kaempferol
*ROS↓, it can counteract pro-oxidants via a number of signaling pathways that either promote the expression of antioxidant enzymes or reduce ROS production.
*Inflam↓, Anti-inflammation activities of Carica papaya.
*AntiDiabetic↑, Anti-diabetes activities of Carica papaya
*neuroP↑, fermented papaya preparation (FPP) exerted neuroprotective properties against copper induced neurotoxicity in Swedish mutant human APP (APPsw) cells
*Wound Healing↑, Wound healing activities of Carica papaya.
*GSH↑, Carica papaya peel extract significantly increased glutathione (GSH), while decreasing MDA and ROS production. Thus, preventing DNA damage and induction of colonic carcinogenesis
*MDA↓,
*DNAdam↓,
*antiOx↑, The antioxidant effect of curcumin was governed by an elevated plasma levels of glutathione peroxidase (GSH) and superoxide dismutase (SOD), improved activity of catalase, and reduced level of lipid peroxidase in plasma.
*GSH↑,
*SOD↑,
*Catalase↑,
*lipid-P↓,
*NF-kB↓, nuclear factor-κB (NF-κB) instigation was significantly inhibited by curcumin followed by the activation of nuclear factor erythroid 2-related factor 2 (Nrf2)
*NRF2↑,
*Wound Healing↑, Similarly, curcumin prorogued the wound-healing activity by declining the levels of lipid peroxides (LPs)
*eff↑, faster wound healing efficiency with a better patient compliance by curcumin mouth wash for managing RT-induced OM
RadioS↑, Although curcumin can sensitize cancer cells to irradiation, healthy cells are much less sensitive to this effect, and thus, curcumin is thought to be a potent, yet safe anti-cancer agent
*radioP↑, curcumin has been found to possess radioprotective properties, since it can lessen inflammatory toxicities associated with radiotherapy, like dermatitis, mucositis, and myelosuppression
EGFR↓, Curcumin can suppress the gene expression of EGFR, and downregulate the TGF-β pathway, thus leading to inhibition of cancer-associated fibroblasts (CAF)
TGF-β↓,
ROS↑, Curcumin can induce ROS generation and suppress DNA repair machinery, thus leading to increased radiation-induced cell death
P53↑, upregulation of both the expression and activity of p53, regulation of the anti-apoptotic PI3K signaling, and suppression of the activity of NF-κB and COX-2
PI3K↓,
NF-kB↓, curcumin increased radiation-induced apoptotic death primarily through inhibition of the NF-κB signaling pathway
COX2↓,
EMT↓, Curcumin was found to suppress radiation-induced EMT resulting in the inhibition of NSCLC migration and invasion
Hif1a↓, inhibition of the expression of both hypoxia-inducible factor 1-alpha (HIF-1a) and heat shock protein 90 (HSP90) proteins and increase in the levels of ROS
HSP90↓,
mTOR↓, In cervical cancer, curcumin has been studied as a potent mTOR inhibitor when given together with irradiation.
*Catalase↑, 40 rats were exposed to curcumin 1 day before irradiation to 3 consecutive days after irradiation, the levels of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA), were found to be considerably eleva
*SOD↑,
*MDA↑,
*Wound Healing↑, treatment with curcumin stimulated wound healing,
*hepatoP↑, curcumin treatment prior to radiation can prevent liver damages, mainly through the modulation of the NF-κB pathway and reduction of oxidative stress (upregulation of SOD, CAD and GSH levels in the curcumin-treated group)
*NF-kB↓,
*ROS↓,
*antiOx↑, Curcumin is a dietary polyphenol and a bioactive phytochemical agent that possesses anti-inflammatory, antioxidant, anticancer, and chemopreventive properties.
*Inflam↓,
AntiCan↑,
chemoPv↑,
*AntiAge↑, antiaging, and neuroprotective as well as wound healing and regenerative effects of curcumin.
*neuroP↑,
*Wound Healing↑,
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other↑, Limonene is an unparalleled terpenoid with numerous therapeutic benefits.
DDS↑, Incorporating it into sophisticated drug delivery systems and medical devices, together with personalised medicine strategies, signifies notable progress in its therapeutic use.
*antiOx↑, graohical abstract
*Inflam↓,
*AntiDiabetic↑,
*neuroP↑,
*Imm↑,
*Wound Healing↑,
*other↑, Limonene can act as a solvent for cholesterol and has, therefore, been used curatively to dissolve gallstones.
*BioAv↑, orally administered D-limonene shows complete absorption from the GI tract of both animals and humans.9
*ROS↓, thereby preventing the further generation of reactive oxygen species (ROS), as depicted in Figure 2
*SOD↑, D-limonene restored the activities of antioxidant enzymes, such as SOD, CAT, GP, and GSH level, further resulting in the reduction of oxidative stress by preventing DNA damage and protein denaturation. T
*Catalase↑,
*GSH↑,
*DNAdam↓,
*AntiDiabetic↑, D-limonene is found to reduce oxidative stress and induce the potentiation of beta cells in the pancreas, thus showing beneficial effects in diabetes mellitus
Casp3↑, D-limonene activates caspases 3 and 9
Casp9↑,
BAX↑, increases the expression of BAX protein, and decreases BCL2 protein expression,
Bcl-2↓,
*AChE↓, Limonene inhibited AChE and BChE activities by 10% and 12%, respectively.
*BChE↓,
*Aβ↓, Limonene decreased Aβ42-induced neuronal cell death and reduced ROS levels, adversely affecting extracellular signal-regulated kinase (ERK) phosphorylation
*ROS↓,
*toxicity?, D-limonene shows low toxicity effects and has not shown much affirmation in animal studies. Some studies have reported that they are non-carcinogenic in humans and do not show much toxicity, even after several years, when administered at low doses.
Apoptosis↑, relatively high electric fields, cell-signaling mechanisms are activated to induce death by apoptosis in cells and tumors.
CA↑, nsPEFs induce calcium release from intracellular stores that mimic physiologic ligand effects on IP3-dependent calcium channels in the endoplasmic reticulum
Wound Healing↑, nsPEF-induced calcium mobilization mimics thrombin-induced platelet activation and aggregation, a natural mechanism to clot blood and heal wounds.
Ca+2↑, leading to an incremental increase in cytoplasmic Ca2+ concentration,
Apoptosis↑, from apoptosis up to cell differentiation and proliferation.
Diff↑,
TumCP↓,
Wound Healing↑, sterilization in the food industry, seed germination, anti-parasitic effects, wound healing, increased immune response
CellMemb↑, available evidence suggest that the increase in cytoplasmic Ca2+ concentration produced by the application of nsPEF could be due to the formation of membrane nanopores.
VGCC↑, most probable cause should be the increase of intracellular Ca2+ concentration via VGCC activation [185].
VGSC↑, findings relating VGNC activation by nsPEF are exciting and deserve more attention.
DNAdam↑, Stacey et al. in 2002 demonstrated that exposing cancer cells to nsPEF with 60 kV/cm could induce DNA damage [243]
selectivity↑, More importantly for nsPEF as cancer treatment, tumor cells are more sensitive to nsPEF than normal cells [246].
Showing Research Papers: 1 to 30 of 30
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 30
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Catalase↓, 1, GSH↓, 1, HO-1↓, 1, lipid-P↓, 1, lipid-P↑, 1, MDA↓, 1, ROS↑, 7, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, MPT↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACSL4↑, 1,
Cell Death ⓘ
Akt↓, 1, APAF1↑, 1, Apoptosis↑, 4, BAX↑, 2, Bcl-2↓, 1, Casp3↓, 1, Casp3↑, 3, Casp9↑, 3, Cyt‑c↓, 1, Cyt‑c↑, 1, iNOS↓, 1, JNK↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↑, 3, other↝, 4, tumCV↓, 2,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, HSP27↓, 1, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3I↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 4, P53↑, 3, P53↝, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 1, Diff↑, 1, EMT↓, 1, ERK↓, 1, mTOR↓, 1, PI3K↓, 2, STAT1↑, 1, TumCG↓, 1, VGCC↑, 1, VGSC↑, 1,
Migration ⓘ
CA↑, 1, Ca+2↑, 1, MMPs↓, 2, TGF-β↓, 1, TJ↓, 1, TumCMig↓, 1, TumCP↓, 3, TumMeta↓, 2, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 3, EGFR↓, 2, EPR↑, 2, HIF-1↓, 1, Hif1a↓, 1, VEGF↓, 1,
Barriers & Transport ⓘ
CellMemb↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IFN-γ↓, 1, IFN-γ↑, 1, IL10↑, 1, IL1β↓, 1, IL2↓, 1, IL2↑, 1, IL4↓, 1, Imm↑, 3, NF-kB↓, 2, NK cell↑, 2,
Cellular Microenvironment ⓘ
cGAS–STING↑, 1,
Protein Aggregation ⓘ
AGEs↓, 1, NLRP3↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 3, ChemoSen↑, 4, DDS↑, 6, Dose↝, 1, eff↓, 1, eff↑, 15, Half-Life↑, 1, RadioS↑, 2, selectivity↑, 2,
Clinical Biomarkers ⓘ
EGFR↓, 2,
Functional Outcomes ⓘ
AntiCan↑, 3, AntiTum↑, 2, chemoPv↑, 2, Obesity↓, 1, toxicity↓, 2, toxicity↝, 1, Wound Healing↑, 8,
Total Targets: 96
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 8, Catalase↑, 4, GPx↑, 1, GSH↓, 1, GSH↑, 3, HDL↑, 1, lipid-P↓, 3, MDA↓, 2, MDA↑, 1, MPO↓, 1, NRF2↑, 1, ROS↓, 7, SOD↑, 5,
Core Metabolism/Glycolysis ⓘ
glucose↓, 1, HMG-CoA↓, 1, LDL↓, 1,
Cell Death ⓘ
Fas↓, 1,
Transcription & Epigenetics ⓘ
AntiThr↑, 1, other↓, 1, other↑, 1, other↝, 2,
DNA Damage & Repair ⓘ
DNAdam↓, 3,
Migration ⓘ
5LO↓, 2, AntiAg↑, 1, Cartilage↑, 1, TGF-β1↓, 1, ZO-1↑, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, CRP↓, 1, DCells↑, 1, IL10↓, 1, IL10↑, 1, IL1β↓, 1, IL6↓, 2, Imm↑, 5, Inflam↓, 10, NF-kB↓, 5, TLR4↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, BChE↓, 1, tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↑, 3, BioAv↝, 1, Dose↝, 1, eff↑, 3, eff↝, 1,
Clinical Biomarkers ⓘ
BP↓, 1, CRP↓, 1, GutMicro↑, 3, IL6↓, 2,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↑, 2, AntiDiabetic↑, 8, Bone Healing↑, 1, cardioP↑, 1, hepatoP↑, 1, neuroP↑, 4, Obesity↓, 1, Pain↓, 1, radioP↑, 1, Risk↓, 2, toxicity?, 1, toxicity↓, 1, toxicity↝, 1, Weight↝, 1, Wound Healing↑, 22,
Infection & Microbiome ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 11, Diar↓, 1,
Total Targets: 74
Scientific Paper Hit Count for: Wound Healing, Wound Healing
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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