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↑,
*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.
*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
*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
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.
*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↓,
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AD, |
NA |
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Park, |
NA |
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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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Var, |
NA |
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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 43 of 43
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 43
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Keap1↑, 1, MFN2↑, 1, ROS↓, 1, ROS↑, 4, ROS⇅, 1, TAC↑, 2, TrxR↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
PPARγ↝, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↑, 4, BAX↑, 1, Casp3↑, 3, cl‑Casp3↑, 1, cl‑Casp3⇅, 1, Casp9↑, 3, Cyt‑c↑, 1, MAPK↝, 1, p38↑, 1, PDCD4↑, 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) ⓘ
TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1, P53↑, 1, PARP↑, 1, cl‑PARP↑, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↑, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, ERK↓, 1, FOXO3↑, 1, mTOR↝, 1, RUNX2↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
TumCI↓, 3, TumCMig↓, 2, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 2, ZBTB10↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, IL6↓, 1, Imm↑, 1, NF-kB↓, 3, PD-L1↓, 1, PGE2↓, 1, TNF-α↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 3, Dose↝, 1, eff↓, 1, eff↑, 5, RadioS∅, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 1, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, AntiTum↑, 1, cardioP↑, 3, chemoP↑, 1, hepatoP↑, 1, neuroP↑, 1, radioP↑, 2, Risk↓, 1,
Total Targets: 69
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, AntiBio↑, 1, Eos↓, 1, GDNF↑, 1, GFAP↓, 1, IgE↓, 1, IL13↓, 1, Learn↑, 2, NeuroI↓, 1, NLR↓, 1, ONOO↓, 1, TRPA1↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, antiOx↑, 14, Catalase↓, 1, Catalase↑, 14, Copper↓, 1, Ferroptosis↓, 1, GPx↑, 11, GPx4↑, 1, GSH↑, 15, GSR↑, 2, GSTA1↑, 1, GSTs↓, 1, GSTs↑, 3, H2O2↓, 2, HO-1↓, 1, HO-1↑, 10, lipid-P↓, 9, MDA↓, 20, MPO↓, 2, NOX4↓, 1, NQO1↑, 3, NRF2↓, 1, NRF2↑, 16, ROMO1↑, 1, ROS↓, 29, SOD↓, 1, SOD↑, 18, SOD1↑, 1, SOD2↑, 1, TAC↑, 41, Thiols↑, 1, TOS↓, 1, TOS↑, 1, TrxR1↑, 1, VitC↑, 1, VitE↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 6, AMPK↑, 2, BUN↓, 2, cAMP↑, 1, CRM↑, 2, glucose↓, 1, GlucoseCon↑, 1, LDH↓, 2, LDH↑, 1, LDL↓, 1, NADPH↑, 1, PKM2↓, 1, PPARγ↓, 1, PPARγ↑, 1, SIRT1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, Akt↑, 1, Apoptosis↓, 3, BAX↓, 1, Bcl-2↑, 2, Casp3↓, 2, Cyt‑c↓, 1, Ferroptosis↓, 1, iNOS↓, 6, MAPK↓, 3, p38↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, other↑, 2,
Protein Folding & ER Stress(tgid=8) ⓘ
NQO2↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3B↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, GSK‐3β↓, 1, PI3K↓, 1, PI3K↑, 1, 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↓, 9,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 3, 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↓, 7, IL8↓, 1, Imm↑, 1, Inflam↓, 19, Inflam↑, 1, MyD88↓, 1, NF-kB↓, 13, PGE2↓, 1, TLR2↓, 2, TLR4↓, 4, TNF-α↓, 12,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 4, BDNF↑, 4, PSD95↑, 1, tau↓, 2, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
AGEs↓, 1, Aβ↓, 7, BACE/β-secretase↓, 3, NLRP3↓, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 4, BioAv⇅, 1, BioAv↝, 2, Dose↑, 1, Dose↝, 6, eff↑, 8, Half-Life↑, 1, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 6, Albumin↑, 1, ALP↓, 1, AST↓, 5, BP↓, 1, creat↓, 2, CRP↓, 2, GutMicro↑, 4, IL6↓, 7, LDH↓, 2, LDH↑, 1, NOS2↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 3, cardioP↑, 6, chemoP↑, 1, cognitive↓, 1, cognitive↑, 6, hepatoP↑, 4, memory↑, 7, neuroP↑, 10, QoL↑, 1, radioP↑, 1, RenoP↑, 5, Strength↑, 1, toxicity↓, 3, toxicity⇅, 1, toxicity↝, 1, toxicity∅, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, AntiViral↑, 1, Bacteria↓, 2, IRF3↓, 1, Sepsis↓, 1,
Total Targets: 190
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:626 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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