antiOx Cancer Research Results
antiOx, anti-oxidant activities: Click to Expand ⟱
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Various antioxidants such as Nrf2, SODs, catalase, GPxs, PRDXs, and GSTs are altered in different cancers and have been linked to prognosis. Their overexpression can correlate with aggressive tumor behavior and resistance to treatment in many contexts.
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Scientific Papers found: Click to Expand⟱
AntiCan↑, All treatments resulted in anticancer effects depicted by cell cycle arrest and apoptosis, with TQ demonstrating greater efficacy than CQ10, both with and without 5-FU.
TumCCA↑,
Apoptosis↑,
eff↑,
Bcl-2↓, However, 5-FU/TQ/CQ10 triple therapy exhibited the most potent pro-apoptotic activity in all cell lines, portrayed by the lowest levels of oncogenes (CCND1, CCND3, BCL2, and survivin)
survivin↓,
P21↑, and the highest upregulation of tumour suppressors (p21, p27, BAX, Cytochrome-C, and Cas-
pase-3).
p27↑,
BAX↑,
Cyt‑c↑,
Casp3↑,
PI3K↓, The triple therapy also showed the strongest suppression of the PI3K/AKT/mTOR/HIF1α pathway, with a concurrent increase in its endogenous inhibitors (PTEN and AMPKα) in all cell lines used.
Akt↓,
mTOR↓,
Hif1a↓,
PTEN↑,
AMPKα↑,
PDH↑, triple therapy favoured glucose oxidation by upregulating PDH, while decreasing LDHA and PDHK1 enzymes.
LDHA↓,
antiOx↓, most significant decline in antioxidant levels and the highest increases in oxidative stress markers
ROS↑,
AntiCan↑, This study is the first to demonstrate the superior anticancer effects of TQ compared to CQ10, with and without 5-FU, in CRC treatment.
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Review, |
AD, |
NA |
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Review, |
Park, |
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*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.
NRF2⇅, 40 nM
BAX↑,
Bcl-2↓,
Fas↑,
MMP↓,
Bax:Bcl2↑,
Cyt‑c↑,
Casp3↑,
Casp12↑,
GSH↓, Allicin can easily penetrate the cell membrane and react with the cellular thiol to transiently deplete the intracellular GSH level, inducing the inhibition of cell cycle progression and growth arrest [98].
TumCCA↑,
ROS↑, An in vitro study indicated that allicin encourages oxidative stress and autophagy in Saos-2 and U2OS (osteosarcoma cells) by modulating the MALATI-miR-376a-Wnt and β-catenin pathway [99].
antiOx↓, As an antioxidant phytochemical, it scavenges reactive oxygen species (ROS) and protects cells from oxidative DNA damage [34].
ROS↑, apoptosis and autophagy pathway in A549 cells by ROS accumulation and facilitating S/G2-M phase arrest in both normoxia as well as hypoxia
HIF-1↓,
E-cadherin↑,
N-cadherin↓,
antiOx↓, ROS trigger cell death when its generation reached toxic threshold level by overcoming the antioxidant capacity of the cell and inducing irreversible oxidative modifications of lipid, protein or DNA [30, 48]
Dose↝, 10μg/ml (LD) and 40μg/ml (HD) allicin for 24hr
Half-Life↝, The pharmacokinetic study demonstrates that a dose of
4 mg/kg in mice results in 2 μM concentration in plasma (with
a half-life of 1.3 h, in the breast cancer model of mice),
Inflam↓, WA has many biological activities: anti-inflammatory (Dubey et al. 2018), immunomodulatory (Davis and Girija 2000), antistress (Singh et al. 2016), antioxidant (Sumathi et al. 2007) and anti-angiogenesis
antiOx↓,
angioG↓,
ROS↑, WA induces oxidative stress (ROS) determining mitochondrial dysfunction as well as apoptosis in leukaemia cells
BAX↑, withaferin mediates apoptosis by ROS generation and activation of Bax/Bak.
Bak↑,
E6↓, The results of the study show that withaferin treatment downregulates the HPV E6 and E7 oncoprotein and induces accumulation of p53 result in the activation of various apoptotic markers (e.g. Bcl2, Bax, caspase-3 and cleaved PARP).
E7↓,
P53↑,
Casp3↑,
cl‑PARP↑,
STAT3↓, WA treatment also decreases the level of STAT3
eff↑, This study concludes that combination of DOX with WA can reduce the doses and side effects of the treatment which gives valuable possibilities for future research.
HSP90↓, by inhibiting the HSP90
TGF-β↓, WA inhibited TGFβ1 and TNFα- induced EMT;
TNF-α↓,
EMT↑,
mTOR↓, by downregulation of mTOR/STAT3 signalling.
NOTCH1↓, WA showed inhibition of pro-survival signalling markers (Notch1, pAKT and NFκB)
p‑Akt↓,
NF-kB↓,
Dose↝, WA dose escalation sets consisted of 72, 108, 144 and 216 mg, fractioned in 2-4 doses/day.
*12LOX↓, The natural product baicalein is a specific inhibitor of 12/15-lipoxygenase, but it also has antioxidant properties.
*antiOx↓,
*neuroP↑, in vivo data suggest that 12/15-lipoxygenase contributes to brain damage after stroke, and that 12/15-LOX inhibition by baicalein is neuroprotective.
*Inflam↓, berberine showed significant memory-improving activities with multiple mechanisms, such as anti-inflammation, anti-oxidative stress, cholinesterase (ChE) inhibition and anti-amyloid effects.
*antiOx↓,
*AChE↓,
*BChE↓, berberine exerts inhibitory effects on the four key enzymes in the pathogenesis of AD: acetylcholinesterase, butyrylcholinesterase, monoamine oxidase A, and monoamine oxidase B
*MAOA↓,
*MAOB↓,
*lipid-P↓, Fig3
*GSH↑,
*ROS↓,
*APP↓,
*BACE↓,
*p‑tau↓,
*NF-kB↓,
*TNF-α↓,
*IL1β↓,
*MAPK↓,
*PI3K↓,
*Akt↓,
*neuroP↑, neuroprotective effects of berberine have been extensively studied
*memory↑, berberine displayed significant effects in preventing memory impairment in these mechanistically different animal models, suggesting an over-all improvement of memory function by berberine
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HCC, |
HUH7 |
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in-vitro, |
HCC, |
H1299 |
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TumCP↓, betulinic acid could suppress proliferation and migration of hepatoma cells, raised ROS level and inhibited antioxidation level in cells
ROS↑,
antiOx↓,
TumCG↓, These findings indicate that betulinic acid has the capacity to significantly impede hepatoma cells growth and migration
TumCMig↓,
NRF2↓, The expression of antioxidant proteins Nrf2, GPX4 and HO-1 was also considerably lower in the BETM and BETH groups than in the Control group
GPx4↓,
HO-1↓,
NCOA4↑, suggesting that betulinic acid activates ferritinophagy by boosting NCOA4 expression and FTH1 degradation.
FTH1↓, betulinic acid groups (10 mg/kg, 20 mg/kg, and 40 mg/kg) greatly boosted LC3II and NCOA4 expressions and suppressed FTH1
Ferritin↑, In summation, betulinic acid decreases antioxidation in tumour tissues from nude mice, inhibits ferritin expression, enhances the expression of ferritinophagy-associated protein, activates ferritinophagy, and initiates ferroptosis in tumour cells.
Ferroptosis↑,
GSH↓, In comparison to the Control group, the betulinic acid groups (10 mg/kg, 20 mg/kg and 40 mg/kg) reduced dramatically GSH and hydroxyl radical inhibition capacity in serum, considerably increased serum Fe2+), and decreased dramatically serum MDA
MDA↓,
Dose↝, results showed that boron supplement is a useful and essential ingredient for humans with a daily intake of about 1-3 mg per day.
Risk↓, Its rich diets have a significant reduction in the risk of developing a variety of cancers including prostate, breast, cervix and lung, liver, melanoma.
*antiOx↓, boron has antioxidant and anti-inflammatory properties
*Inflam↓,
ChemoSen↑, Boron-containing compounds indicate promising effects for chemotherapy types of cancer.
AntiCan↑, Compounds of boron, which have an anticancer effect, include boric acid, borate, borate esters, boranes, borinic esters (26). Boric acid is one of the most studied boron-containing chemicals.
*PCNA↓, Boron reduced PCNA and ameliorated oxidative stress in rats exposed to cancer
*ROS↓,
other↝, Physicians should be encouraged to more routinely discuss supplements use with their cancer patients and increase of clinical research on boron and cancer prevention seems necessary.
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in-vivo, |
IBD, |
NA |
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in-vivo, |
Park, |
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*GutMicro↑, Carvacrol can regulate the gut microbiota. bundance of specific microbiota, such as Lactobacillus, Escherichia coli/Shigella, and Lachnoclostridium.
Risk↓, Carvacrol inhibits the development of colitis-associated colorectal cancer.
*Inflam↓, nti-inflammatory and antioxidant traits,
*antiOx↓,
*ZO-1↑, carvacrol significantly restored colonic length (p < 0.01) and re-established key tight junction proteins like ZO-1.
*iNOS↓, downregulated mRNA levels of inflammatory mediators such as iNOS and IL-6.
*IL6↓,
*NO↓, carvacrol has been shown to suppress nitric oxide and prostaglandin E2 production
*PGE2↓,
*memory↑, carvacrol improves memory deficits in Parkinson’s disease models
*TLR4↓, anti-inflammatory effects of carvacrol by inhibiting the TLR4/NF-κB signaling pathway
*NF-kB↓,
*IBI↑, Carvacrol improves intestinal barrier function
*CLDN3↑, expression levels of ZO-1, Claudin3, Claudin1, Occludin, and Mucin were significantly increased in the carvacrol group compared to the DSS group
*CLDN1↑,
*MUC1↑,
*OCLN↑,
*iNOS↑, carvacrol significantly inhibited the mRNA expression levels of iNOS, COX-2, Interferon-γ, IL-1β, and IL-6 in the intestinal tracts of colitis mice
*COX2↓,
*IFN-γ↓,
IL1β↓,
ADAM10?,
AntiCan↑, chlorogenic acid (CHA) possesses several pharmacological attributes, such as anticancer, hepatoprotective, antimicrobial, immune-suppressant, antioxidant, and antidiabetic activities.
*hepatoP↑,
*Bacteria↓,
*antiOx↓,
*AntiDiabetic↑,
Apoptosis↓, It can hinder the process of cell division, trigger cell apoptosis, and suppress an increase in cancerous cell growth.
TumCG↓,
angioG↓, mechanisms include angiogenesis, invasion and migration, oxidative stress, inflammation, cell cycle arrest, and proliferation.
TumCI↓,
TumCMig↓,
ROS↝,
Inflam↝,
*Dose↝, 6-month intake of a test beverage containing 330 mg of CGAs just before bedtime(dissolved in 100 mL of water)caffeine level of the test beverage was below the limit of quantification (<1 mg/100 g)
*memory↑, A 6-month intake of CGAs may improve attentional, executive, and memory functions in the elderly with complaints of subjective memory loss.
*Risk↓, High intake of fruits, vegetables, fish, nuts, and legumes and low intake of meat, high fat dairy, and sweets have been shown to delay aging-related cognitive impairment and reduce the risk of Alzheimer's disease (AD)
*cognitive↑, Improved cognitive function as a result of drinking coffee is thought to be mediated by caffeine and chlorogenic acids (CGAs).
*Aβ↓, CGAs protect neurons and suppress the aggregation of Aβ through antioxidative effects [12, 13].
*antiOx↓,
*motorD↑, Motor speed 92.5 ± 5.2 98.4 ± 7.7
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
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Pca, |
LNCaP |
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Pca, |
PC3 |
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MMP9↓, MMP-9
activity is significantly inhibited by curcumin with less effect
on MMP-2.
Matr↓, Fig. 2C, curcumin proficiently decreased the total levels of matriptase including latent matriptase (70kDa) and activated matriptase (a 120 kDa complex of activated matriptase and its cognate inhibitor HAI-1) in a dose-dependent manner.
Inflam↓, The antiinflammatory and antioxidant activities of curcumin have been proposed via inhibiting NF-kB,COX-2, iNOS, and cytokine production (9, 10).
antiOx↓,
NF-kB↓,
COX2↓,
iNOS↓,
TumCMig↓, Curcumin inhibition of prostate cancer cell migration
and invasion
TumCI↓,
*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage
*Inflam↓, present in fruits and vegetables such as strawberries, apple, cucumber, persimmon, grape and onion, was shown to possess anti-microbial, anti-inflammatory, anti-oxidant
*antiOx↓, fisetin possesses stronger oxidant inhibitory activity than well-known potent antioxidants like morin and myricetin.
*ERK↑, inducing extracellular signal-regulated kinase1/2 (ERK)/c-myc phosphorylation, nuclear NF-E2-related factor-2 (Nrf2), glutamate cystine ligase and glutathione (GSH) levels
*p‑cMyc↑,
*NRF2↑,
*GSH↑,
*HO-1↑, activate Nrf2 mediated induction of hemeoxygenase-1 (HO-1) important for cell survival
mTOR↓, in our studies on fisetin in non-small lung cancer cells, we found that fisetin acts as a dual inhibitor PI3K/Akt and mTOR pathways
PI3K↓,
Akt↓,
TumCCA↑, fisetin treatment to LNCaP cells resulted in G1-phase arrest accompanied with decrease in cyclins D1, D2 and E and their activating partner CDKs 2, 4 and 6 with induction ofWAF1/p21 and KIP1/p27
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
P21↑,
p27↑,
JNK↑, fisetin could inhibit the metastatic ability of PC-3 cells by suppressing of PI3 K/Akt and JNK signaling pathways with subsequent repression of matrix metalloproteinase-2 (MMP-2) and MMP-9
MMP2↓,
MMP9↓,
uPA↓, fisetin suppressed protein and mRNA levels of MMP-2 and urokinase-type plasminogen activator (uPA) in an ERK-dependent fashion.
NF-kB↓, decrease in the nuclear levels of NF-B, c-Fos, and c-Jun was noted in fisetin treated cells
cFos↓,
cJun↓,
E-cadherin↑, upregulation of E-cadherin and down-regulation of vimentin and N-cadherin.
Vim↓,
N-cadherin↓,
EMT↓, EMT inhibiting potential of fisetin has been reported in melanoma cells
MMP↓, The shift in mitochondrial membrane potential was accompanied by release of cytochrome c and Smac/DIABLO resulting in activation of the caspase cascade and cleavage of PARP
Cyt‑c↑,
Diablo↑,
Casp↑,
cl‑PARP↑,
P53↑, fisetin with induction of p53 protein
COX2↓, Fisetin down-regulated COX-2 and reduced the secretion of prostaglandin E2 without affecting COX-1 protein expression.
PGE2↓,
HSP70/HSPA5↓, It was shown that the induction of HSF1 target proteins, such as HSP70, HSP27 and BAG3 were inhibited in HCT-116 cells exposed to heat shock at 43 C for 1 h in the presence of fisetin
HSP27↓,
DNAdam↑, DNA fragmentation, an increase in the number of sub-G1 phase cells, mitochondrial membrane depolarization and activation of caspase-9 and caspase-3.
Casp3↑,
Casp9↑,
ROS↑, This was associated with production of intracellular ROS
AMPK↑, Fisetin induced AMPK signaling
NO↑, fisetin induced cytotoxicity and showed that fisetin induced apoptosis of leukemia cells through generation of NO and elevated Ca2+ activating the caspase
Ca+2↑,
mTORC1↓, Fisetin was shown to inhibit the mTORC1 pathway and its downstream components including p70S6 K, eIF4B and eEF2 K.
p70S6↓,
ROS↓, Others have also noted a similar decrease in ROS with fisetin treatment.
ER Stress↑, Induction of ER stress upon fisetin treatment, evident as early as 6 h, and associated with up-regulation of IRE1, XBP1s, ATF4 and GRP78, was followed by autophagy which was not sustained
IRE1↑,
ATF4↑,
GRP78/BiP↑,
eff↑, Combination of fisetin and the BRAF inhibitor sorafenib was found to be extremely effective in inhibiting the growth of BRAF-mutated human melanoma cells
eff↑, synergistic effect of fisetin and sorafenib was observed in human cervical cancer HeLa cells,
eff↑, Similarly, fisetin in combination with hesperetin induced apoptosis
RadioS↑, pretreatment with fisetin enhanced the radio-sensitivity of p53 mutant HT-29 cancer cells,
ChemoSen↑, potential of fisetin in enhancing cisplatin-induced cytotoxicity in various cancer models
Half-Life↝, intraperitoneal (ip) dose of 223 mg/kg body weight the maximum plasma concentration (2.53 ug/ml) of fisetin was reached at 15 min which started to decline with a first rapid alpha half-life of 0.09 h and a longer
half-life of 3.12 h.
TumCG↓, Fisetin has shown the ability to suppress tumor growth and metastasis by modulating critical signaling pathways, including PI3K/Akt/mTOR, NF-κB, and MAPK.
ER Stress↑, It induces apoptosis in cancer cells through mitochondrial and endoplasmic reticulum stress responses and demonstrates antioxidative properties by reducing reactive oxygen species.
antiOx↓,
ROS↓,
ChemoSen↑, Additionally, fisetin enhances the efficacy of conventional chemotherapies, indicating its role as a potential adjuvant in cancer treatment.
antiOx↓, Lycopene is a potent antioxidant that fights ROS and, subsequently, complications.
ROS↓,
BP↓, It reduces blood pressure via inhibiting the angiotensin-converting enzyme and regulating nitrous oxide bioavailability.
LDL↓, important role in lowering of LDL (low-density lipoproteins) and improving HDL (high-density lipoproteins) levels to minimize atherosclerosis
*toxicity∅, Lycopene is a natural substance that may be used in high doses as a dietary supplement without causing harm to human health or physiology
eff↑, Thermal food processing, particularly in the presence of cooking oils, causes lycopene to micellize and enhance its intestinal absorption rate by a factor of ten
ROS↑, As a pro-oxidant, lycopene may have both good and negative impacts in biological systems, as well as influence the course of human illnesses.
*Half-Life↑, Plasma lycopene has a half-life of 12–33 days in the human body
*BioAv↓, Tomato lycopene is not easily absorbed since it is integrated into the nutritional matrix.
*BioAv↑, Clinical research demonstrates that heat-processed tomato products absorb lycopene more quickly than raw sources, and that adding oil increases absorption
*antiOx↑, Lycopene’s ability to protect against oxidative stress has been established
AntiCan↑, The anticancer potential of lycopene has been described by various in vitro cells, animal studies, and some clinical trials.
antiOx↓, anticancer potential of lycopene is mainly due to its powerful singlet-oxygen quencher characteristics, simulation of detoxifying/antioxidant enzymes production,
Apoptosis↓, initiation of apoptosis, inhibition of cell proliferation and cell cycle progression as well as modulations of gap junctional communication, the growth factors, and signal transduction pathways
TumCP↓,
TumCCA↑,
Risk↓, The link between increased lycopene consumption and reducedoccurrence of a variety of cancers has been documented by in vitro cells,animal studies, and some clinical studies.
ROS↓, The antioxidant action of lycopene toward ROS
SOD↑, Lycopene can simulate detoxifying/antioxidant enzyme productionsuch as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), and glutathione reductase.
Catalase↑, . By stimulating ARE system, the lycopene can increase detoxifying/antioxidant enzymes production such as SOD, CAT, GST
GSTs↑,
ARE↑, The upregulating of the ARE system by lycopere has been studied in human BEAS-2B, HepG2, and MCF7
NRF2↑, figure 1
cycD1/CCND1↓, figure 2
cycE/CCNE↑,
CDK2↑,
p27↑,
BAX↑,
Bcl-2↓,
P53↑,
ChemoSen↑, Lycopene has also been declared to have a synergistic effect with drugs used in cancer treatment [16,17,27,32]. Lycopene may contribute to improved anticancer effects of enzalutamide
ROS↑, Magnolol promotes the production of reactive oxygen species (ROS) and inhibits the antioxidant pathway in cancer cells.
antiOx↓,
mtDam↑, leading to mitochondrial dysfunction and mitocytosis
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*ROS↓, melatonin and its metabolic derivatives possess strong free radical scavenging properties.
*antiOx↓, potent antioxidants against both ROS (reactive oxygen species) and RNS (reactive nitrogen species). reduce oxidative damage to lipids, proteins and DNA under a very wide set of conditions where toxic derivatives of oxygen are known to be produced.
ROS↑, a few studies using cultured cells found that melatonin promoted the generation of ROS at pharmacological concentrations (μm to mm range) in several tumor and nontumor cells; thus, melatonin functioned as a conditional pro-oxidant.
selectivity↑, melatonin functions as a prooxidant in cancer cells where it aids in the killing of tumor cells
Dose↑, Melatonin levels in the nucleus and mitochondria reached saturation with a lower dose of 40 mg/kg body weight, with no further accumulation under higher doses of injected melatonin
*mitResp↑, improves mitochondrial respiration and ATP production, thereby reducing electron leakage and ROS generation
*ATP↑,
*ROS↓,
eff↑, melatonin protects mitochondrial function in the brain of Alzheimer's patients through both MT1/MT2 dependent and independent mechanisms
ROS↑, Cytochrome P450 utilizes melatonin as a substrate to generate ROS in mitochondria (melatonin concentration
ranges from 0.1 to 10 uM)
Dose↑, melatonin at high concentrations (10-1000uM ) was able to promote ROS generation and lead to Fas-induced apoptosis in human leukemic Jurkat cells. Concentrations of <10uM , melatonin did not induce significant ROS generation in these cancer cells
*toxicity∅, High levels of melatonin (uM to mM) did not cause cytotoxicity in several types of nontumor cells
ROS↑, lower concentrations of melatonin (0.1-10uM ), which exhibited antioxidant action in HepG2 cells within 24 hr, became pro-oxidant after 96 hr of treatment, as indicated by the increase of GSH with 24hr and depletion after 96 hr.
eff↓, Finally, a compound, chlorpromazine, which specifically interrupts the binding of melatonin to calmodulin [188], prevented melatonin-induced AA release and ROS generation;
ROS↝, It remains unknown whether the pro-oxidant action exists in vivo. the vast majority of evidence indicates that melatonin is a potent antioxidant in vivo even at pharmacological concentrations
Dose↑, decline of melatonin production with age may render it more beneficial to supplement melatonin to the aging population to improve health by reducing free radical damage
other↑, melatonin intake has the potential to improve cardiac function, inhibit cataract formation, maintain brain health, alleviate metabolic syndrome, obesity and diabetes,reduce tumorigenesis, protect tissues against ischemia
*Inflam↓, including anti-inflammatory, antioxidant, neuroprotective, hepatoprotective, and anti-cancer activities
*antiOx↓,
neuroP↑, neuroprotective
hepatoP↑, hepatoprotective
AntiCan↑,
Apoptosis↑, apoptosis induction, cell cycle arrest, angiogenesis hindrance
TumCCA↑,
angioG↓,
ROS↝, antioxidant effects, by modulating reactive oxygen species (ROS) levels and increasing superoxide dismutase (SOD
SOD↑,
TGF-β↓, inhibition of transforming growth factor-β (TGF-β), suppression of regulatory T-cells (Tregs), and down-regulation of interleukin-1β (IL-1β)
Treg lymp↓,
IL1β↓,
*BioAv↝, naringenin is mainly responsible for its low aqueous solubility, low oral bioavailability, and instability which are challenges to its efficient medical application. To overcome these physicochemical issues, nano-drug delivery systems have been used
ChemoSen↑, ombinational therapy consisting of naringenin and standard anti-cancer agents is arising, as a new treatment strategy and was proven to show synergistic effects
cardioP↑, cardioprotective
Inflam↓, anti-inflammatory, antioxidant, antiapoptotic, anticancer and antiulcer effects
antiOx↓,
AntiCan↑,
BioAv↓, clinical application of naringin is severely restricted due to its susceptibility to oxidation, poor water solubility, and dissolution rate. low bioavailability (approximately 8.8%) when administered orally
BioAv↓, In addition, naringin shows instability at acidic pH, is enzymatically metabolized by β-glycosidase in the stomach and is degraded in the bloodstream when administered intravenously
BioAv↑, limitations, however, have been overcome thanks to the development of naringin nanoformulations.
INF-γ↓, The report indicates decreased levels of proinflammatory cytokines (INF-γ, IL-6, and TNF-α) with an increase in IL-10 (anti-inflammatory cytokine), and the attenuation of serum rheumatoid factor (RF-factor) levels and C-reactive protein (CRP)
IL6↓,
TNF-α↓,
IL10↑,
CRP↓,
BioAv↓, We provide an in-depth analysis of OC’s poor bioavailability
*Inflam↓, well-characterized anti-inflammatory and antioxidant effects
*antiOx↓,
cMET↓, inhibition of key oncogenic signaling pathways (c-MET/STAT3, PAR-2/TNF-α, COX-2/mPGES-1)
STAT3↓,
TNF-α↓,
COX2↓,
EMT↓, the suppression of epithelial-to-mesenchymal transition (EMT), angiogenesis, and metabolic reprogramming
angioG↓,
*GutMicro↝, OC’s bidirectional interaction with gut microbiota
eff↑, OC’s significant potential in combination therapies, detailing its synergistic interactions with standard treatments (e.g., PARP inhibitors, taxanes, FLT3 inhibitors)
ChemoSen↑, Ingredients from propolis also ”sensitize“ cancer cells to chemotherapeutic agents
TumCCA↑, cell-cycle arrest and attenuation of cancer cells proliferation
TumCP↓,
Apoptosis↑,
antiOx↓, behave as antioxidants against peroxyl and hydroxyl radicals,
ROS↑, whereas prooxidant activity is observed in the presence of Cu2+.
COX2↑, Propolis, as well as flavonoids derived from propolis, such as galangin, is a potent COX-2 inhibitor
ER(estro)↓, Some flavonoids from propolis, such as galangin, genistein, baicalein, hesperetin, naringenin, and quercetin, suppressed the proliferation of an estrogen receptor (ER)
cycA1/CCNA1↓, by suppressing expressions of cyclin A, cyclin B, and Cdk2 and by stopping proliferation at the G2 phase, by increasing levels of p21 and p27 proteins, and through the inhibition of telomerase reverse transcriptase (hTERT),
CycB/CCNB1↓,
CDK2↓,
P21↑,
p27↑,
hTERT/TERT↓, leukemia cells, propolis successfully reduced hTERT mRNA expression
HDAC↓, by suppressing expressions of cyclin A, cyclin B, and Cdk2 and by stopping proliferation at the G2 phase, by increasing levels of p21 and p27 proteins, and through the inhibition of telomerase reverse transcriptase (hTERT),
ROS⇅, Mexican propolis, demonstrated both pro- and anti-inflammatory effects, depending on the dose applied
Dose?, Mexican propolis, demonstrated both pro- and anti-inflammatory effects, depending on the dose applied
ROS↓, By scavenging free radicals, chelating metal ions (mainly iron and copper), and stimulating endogenous antioxidant defenses, propolis and its flavonoids directly attenuate the generation of ROS
ROS↑, Romanian propolis [99], exhibits prooxidant properties at high concentrations, by mobilizing endogenous copper ions and DNA-associated copper in cells.
DNAdam↑, propolis, i.e., its polyphenolic components, may induce DNA damage in the presence of transition metal ions.
ChemoSen↑, Algerian propolis + doxorubicin decreased cell viability, prevented cell proliferation and cell cycle progression, induced apoptosis by activating caspase-3 and -9 activities, and increased the accumulation of chemotherapeutic drugs in MDA-MB-231 cel
LOX1↓, propolis components inhibited the LOX pathway
lipid-P↓, Croatian propolis improved psoriatic-like skin lesions induced by irritant agents n-hexyl salicylate or di-n-propyl disulfide by decreasing the extent of lipid peroxidation
NO↑, Taken together, propolis may increase the phagocytic index, NO production, and production of IgG antibodies
Igs↑,
NK cell↑, propolis treatment for 3 days increases the cytotoxic activity of NK cells against murine lymphoma.
MMPs↓, extracts of propolis containing artepillin C and CAPE decreased the formation of new vessels and expression of MMPs and VEGF in various cancer cells
VEGF↓,
Hif1a↓, Brazilian green propolis inhibit the expression of the hypoxia-inducible factor-1 (HIF-1) protein and HIF-1 downstream targets such as glucose transporter 1, hexokinase 2, and VEGF-A
GLUT1↓,
HK2↓,
selectivity↑, Portuguese propolis was selectively toxic against malignant cells.
RadioS↑, propolis increased the lifespan of mice that received the radiotherapy with gamma rays
GlucoseCon↓, Portuguese propolis disturbed the glycolytic metabolism of human colorectal cancer cells, as evidenced by a decrease in glucose consumption and lactate production
lactateProd↓,
eff↓, Furthermore, different pesticides or heavy metals can be found in propolis, which can cause unwanted side effects.
*BioAv↓, Due to the low bioavailability and clinical efficacy of propolis and its flavonoids, their biomedical applications remain limited.
TumCP↓, data revealed that piperine markedly repressed cell proliferation and migration, and induced apoptosis in PCa DU145.
TumCMig↓,
Apoptosis↑,
p‑Akt↓, piperine reduced the expression of p-Akt, MMP-9 and p-mTOR.
MMP9↓,
p‑mTOR↓,
TumMeta↓, therapeutic agent to better overcome PCa metastasis
*antiOx↓, piperine has an extensive pharmacological properties, such as antioxidant (7), anti-inflammatory (8,9), hepatoprotective (10), antimicrobial (11,12), immunomodulatory and anticancer
*Inflam↓,
*hepatoP↑,
*Imm↑,
*AntiCan↑,
Apoptosis↑, piperine exposure induces apoptosis significantly in a dose-dependent manner and inhibits the growth of HeLa cells with an increase in ROS generation,
TumCG↓,
ROS↑,
MMP↓, piperine also encourages cell death by the loss of MMP, DNA fragmentation and the activation of caspase-3
DNAdam↑,
Casp3↑,
TumCCA↑, Growth inhibition of HeLa cells was found to be associated with G2/M phase arrest and sub-G1 accumulation.
*Inflam↓, Piperine possesses multifunctional pharmacological properties such as anti-inflammatory, antioxidant, antidiarrheal, hypolipidemic, hepato-protective, anti-mutagenic, antimicrobial and anti-carcinogenic activities
*antiOx↓,
*hepatoP↑,
ChemoSen↑, Dietary piperine has been shown to increase the therapeutic effect of docetaxel against castration-resistant prostate cancer in xenograft animal models
CSCs↓, Piperine has inhibited the growth of breast carcinoma by targeting the renewal of cancer stem cells
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*antiOx↓, Firstly, pterostilbene act as an antioxidant against various free radicals,
*ROS↑, reducing ROS production
*SOD↑, as well as increasing SOD and glutathione (GSH) activation via the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway in neuronal cells [44].
*GSH↑,
*NRF2↑, by activating Nrf2
*MDA↓, pterostilbene reduced malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), aconitase-2 and 8-hydroxydeoxyguanosine (8-OHdG) level;
*HNE↓,
*Inflam↓, Pterostilbene has been reported as a potential anti-
inflammatory agent
*MAPK↓, pterostilbene inhibited mitogen-activated protein kinase (MAPK) activation and the production of pro-inflammatory cytokine (interleukin-6 [IL-6] and TNF-a)
*IL6↓,
*TNF-α↓,
*HO-1↑, through upregulating heme
oxygenase-1 (HO-1) to prevent hypoxic-ischemic brain injury
in neonatal rats
*cardioP↑, beneficial health effects of resveratrol and pterostilbene on cardioprotection, neuroprotection
*neuroP↑,
*CRM↑, as a calorie restriction mimic
*NLRP3↓, nhibiting pro-inflammatory cytokine such as IL-1b and NLRP3 inflammasome activation,
*Apoptosis↓, 40 μM quercetin improved cell viability, reduced apoptosis, and preserved cell functions.
*ROS↓, Quercetin also decreased reactive oxygen species (ROS) levels in TM4 cells exposed to FB1
*antiOx↓, enhanced the expression of antioxidant genes
*MMP↑, improved mitochondrial membrane potential.
*GPI↑, elevated the mRNA and protein expression of glycolysis-related genes, including (Gpi1), (Hk2), (Aldoa), (Pkm), lactate (Ldha) and (Pfkl)
*HK2↑,
*ALDOA↑,
*PKM1↑,
*LDHA↑,
*PFKL↑,
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*BG↓, Two doses of quercetin increased rat body weight and testicular weight, decreased blood glucose, and inhibited oxidative stress.
*ROS↓,
*SOD↑, Both doses of quercetin reduced reactive oxygen species and malondialdehyde levels, and increased superoxide dismutase level in HG-treated cells.
*MDA↓,
*ER Stress↓, quercetin inhibits endoplasmic reticulum stress
*iNOS↓, Quercetin could eliminate the upregulation of iNOS, ET-1, and AR mRNA levels in HG-treated cells
*CHOP↓, HG treatment increased CHOP and Grp78 mRNA and protein levels in HG-treated cells, and two doses (5 or 10 μM) of quercetin all decreased these levels
*GRP78/BiP↓,
*antiOx↓, Quercetin is a natural polyphenol compound with anti-inflammatory [37], anti-oxidant [38], and blood sugar lowering properties
*Inflam↓,
*JAK2↑, Our results in vitro showed that quercetin treatment upregulated the phosphorylation levels of JAK2 and STAT3 in HG treated cells. (activating of the JAK2/STAT3 pathway could inhibit ER stress)
*STAT3?,
AntiAg↑, The degree of platelet adhesion decreased by increasing the resveratrol concentration.
antiOx↓, but it seems to be related to its antioxidant activity, its ability to inhibit ribonucleotide reductase, DNA polymerase and cyclooxygenase 2 (COX-2)
COX2↓,
antiOx↓, SFN is a bioactive compound with both antioxidant and anti-inflammatory properties.
Inflam↓,
ChemoSen↑, SFN also improves the efficacy of certain traditional chemotherapeutic regimens
ROS⇅, A lesser established mechanism proposed by Li, et al. is that SFN induces mild increases ROS, leading to transcription factor EB (TFEB) activation. TFEB plays a role in activating antioxidant response elements and...ultimately reducing overall oxidat
*NRF2↑, SFN treatment increased Nrf2 and, therefore, glutathione levels
*GSH↑,
Catalase↑, Cancer cells treated with SFN showed higher catalase levels, heme oxygenase 1, and NAD(P)
HO-1↑,
NAD↑,
chemoP↑, Taken together, these studies provide strong evidence for the chemoprotective nature of SFN in various human epithelial cancers, including those of the bladder.
*neuroP↑, silymarin is employed significantly as a neuroprotective, hepatoprotective, cardioprotective, antioxidant, anti-cancer, anti-diabetic, anti-viral, anti-hypertensive, immunomodulator, anti-inflammatory, photoprotective and detoxification agent
*hepatoP↑,
*cardioP↑,
*antiOx↓,
*NLRP3↓, Zhang et al. (2018) observed that silybin significantly impedes NLR family pyrin domain containing 3 (NLRP3) inflammasome activation in NAFLD by elevating NAD+ levels,
*NAD↑,
ROS↓, MDA-MB-231: it was observed that silybin treatment also abolishes activation of the NLRP3 inflammasome through repression of ROS generation, resulting in reduced tumor cell migration and invasion
NLRP3↓,
TumCMig↓,
*COX2↓, mpairing several enzymes (COX-2, iNOS, SGPT, SGOT, MMP, MPO, AChE, G6Pase, MAO-B, LDH, Telomerase, FAS and CK-MB)
*iNOS↓,
*MPO↓,
*AChE↓,
*LDH↓,
*Telomerase↓,
*Fas↓,
Inflam↓, Silymarin was reported to possess anti-inflammatory, antioxidant, and neuroprotective impacts.
antiOx↓,
neuroP↑,
cognitive↑, recent study shed light on the neuroprotective attributes of silymarin against cognitive dysfunction instigated in rats with doxorubicin/cyclophosphamide combination
NRF2↑, additionally, caspase-3 augmentation and of nuclear factor erythroid 2-related factor-2 (Nrf-2) and heme oxygenase-1 (HO-1) pathway disturbance were found following chemotherapy treatment.
HO-1↑,
memory↑, Silymarin treatment opposed such effects via enhancing memory function, preserving brain architecture, and reducing acetylcholinesterase activity and caspase-3 level.
AChE↓,
Casp3↓,
*hepatoP↑, Silibinin (silybin), a flavonoid derived from the herb milk thistle, is well known for its hepatoprotective activities.
*neuroP↑, neuroprotective effect of silibinin on Aβ25-35-injected rats
*cognitive↑, silibinin significantly attenuated Aβ25-35-induced memory deficits in Morris water maze and novel object-recognition tests.
*memory↑,
*Inflam↓, Silibinin attenuated the inflammatory responses, increased glutathione (GSH) levels and decreased malondialdehyde (MDA) levels, and upregulated autophagy levels in the Aβ25-35-injected rats.
*GSH↑,
*MDA↓,
*Inflam↓, potential candidate for AD treatment because of its anti-inflammatory, antioxidant and autophagy regulating activities.
*antiOx↓,
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*antiOx↓, Functions of selenium are diverse as antioxidant, anti-inflammation, increased immunity, reduced cancer incidence, blocking tumor invasion and metastasis, and further clinical application as treatment with radiation and chemotherapy.
*Inflam↓,
Risk↓,
TumCI↓,
TumMeta↓,
radioP↑,
chemoP↑,
Apoptosis↑, (SeDG), which induces cytotoxicity as cell apoptosis, ROS production, DNA damage, and adenosine-methionine methylation in the cellular nucleus
ROS↑,
DNAdam↑,
Dose↑, In our study, advanced cancer patients can tolerate until 5000 μg of sodium selenite in combination with radiation and chemotherapy since the half-life of sodium selenite may be relatively short
selectivity↑, selenium may accumulates more in cancer cells than that of normal cells, which may be toxic to the cancer cells.
*other↓, Se-methylselenocysteine (MSeC) is most abundant in garlic, broccoli, walnut, and some other plant products.
*BioAv↑, Most Se compounds are readily absorbed from the diet and are mainly metabolized in the liver.
ROS↑, Methylselenol induced apoptosis by ROS production, subsequently altered mitochondrial membrane potential, and, further, induced caspases’ activity.
MMP↓,
Casp↑,
*Imm↑, Se activates immune functions via the activation of IL-2 receptor [59].
*Pain↓, Supplementation with 200 μg Se in a group of rheumatoid arthritis patients for three months significantly reduced pain and joint involvement
Sepsis↓, Se plays an important role in defense against acute illness, such as sepsis syndrome
MMP2↓, Several experiments by our group demonstrate that selenite inhibits tumor invasion by blocking MMP-2 and -9 expression
MMP9↓,
*Half-Life↓, a short half-life of sodium selenite and more accumulation of the Se in the cancer cells may be more toxic in cancer cells than that in normal cells.
*ROS↓, In this study, TQ-NLC or TQ was seen to reduce the level of ROS produced in the cells at all concentrations of treatment given.
*antiOx↓, Both of these compounds are able to exert their antioxidant activity at the concentration as lower as 3 μM within 24 hours of treatment and as higher as 12 μM without causing any harm towards the cells.
*BioAv↓, bioavailability of TQ is limited by its poor solubility and lipophilic nature in water
*BioAv↑, to overcome the disadvantages of TQ, thymoquinone-loaded nanostructured lipid carrier (TQ-NLC) was designed and effectively prepared by Ng et al. [49] via high-pressure homogenization technique
*NO↑, TQ was also reported to decrease production of nitric oxide (NO) and attenuate nitrosative stress by inhibiting the inducible nitric oxide synthase enzyme
*SOD↑, TQ exhibits strong antioxidant activity by upregulating superoxide dismutase (SOD), glutathione (GPX), and catalase (CAT) [88].
*GPx↑,
*Catalase↑,
*GSH↑, TQ restored the decrease in the intracellular antioxidant enzyme glutathione levels and inhibited the generation of reactive oxygen species induced by Aβ1–42.
*ROS↓,
*neuroP↑, Thus, the findings of our study suggest that TQ holds a neuroprotective potential and could be a promising therapeutic agent to reduce the risk of developing AD and other disorders of the central nervous system.
*Casp3↓, Aβ1–42 (5 μM) induced about 90% increase in the caspase 3/7 activities (**P < 0.01). However, TQ (100 nM) co-treatment restored caspase 3/7 activities to control sample level
*Casp7↓,
*antiOx↓, strong antioxidant capabilities, TQ has been demonstrated to protect the brain and the spinal cord from oxidative damage generated by different pathologies induced by a variety of free radicals
*H2O2↓, Intriguingly, the co-treatment with TQ restored the content of GSH and significantly inhibited the apparent increase in H2O2.
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*Inflam↓, its anti-inflammatory, anti-oxidant, and anti-apoptotic properties.
*antiOx↓,
*neuroP↑, potential applications of UA in neuroprotective strategies
*p‑tau↓, mainly in AD and ischemic neuronal injury resulting in improved cognition, reduced neuroinflammation, neuronal loss, tau phosphorylation, and amyloid plaques
*Aβ↓,
*eff↑, The bioavailability of ellagitannin is very low; however, their absorption may be increased by the co-intake of dietary fructooligosaccharides.
*BioAv↓, only 40% of individuals could naturally convert the polyphenolic precursors to UA
*BioAv↑, administration of UA is proposed to be an answer for urolithin non-producers, which could allow for the exploration of its health benefits
*GSH↑, UA administration protected against the cisplatin-induced depletion of the renal GSH pool, the inhibition of GPx and superoxide dismutase (SOD) activity
*SOD↑,
*lipid-P↓, declined lipid peroxidation and protein nitration were observed
*Catalase↑, UA not only enhanced the cellular antioxidant mechanism attributed to increased CAT, SOD, glutathione reductase (GR), and GPx activity, but also inhibited oxidizing enzymes contributing to reactive oxygen species (ROS)
*GSR↑,
*GPx↑,
*ROS↓,
*NRF2↑, Beneficial effects of UA, including antioxidant activity, are believed to be mediated through the activation of the Nrf2/Kelch-like ECH-associated protein 1 (Keap1) signaling pathway
*GutMicro↑, enhancing the gut barrier integrity caused by the UA administration
*Risk↓, Urine UA elevation was reported to also be associated with decreased age-related hippocamp atrophy—a biomarker of neurodegeneration and cognitive decline
*BBB↓, free form of UA crossing the blood–brain barrier (BBB) in animal model studies
*NLRP3↓, UA downregulated NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome-mediated inflammation,
*MAOA↓, Another aspect of the role of UA in PD management is its inhibitory effects on monoamine oxidase (MAO).
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BioAv↝, Urolithin A (UA), a metabolite derived from ellagic acid through gut microbiota metabolism, has emerged as a compelling anticancer agent.
TumAuto↝, UA has multiple mechanisms of action, including the regulation of autophagy, enhancement of mitochondrial function, and inhibition of tumor progression and metastatic pathways.
TumCG↓,
TumMeta↓,
ChemoSen↑, Additionally, its chemo-, immuno-, and radio-sensitization properties further increase its therapeutic advantages
Imm↑,
RadioS↑,
BioAv↑, Nanotechnology-driven approaches, such as nanoparticle formulations, lipids, and powder formulations, have successfully increased the solubility, stability, bioavailability, precise targeted delivery to cancer tissues
other↝, While sparingly soluble in water, UA shows better solubility in organic solvents, such as ethanol and dimethyl sulfoxide.
eff↓, prone to degradation at extreme pH values or high temperatures.
*antiOx↓, UA has gained increasing attention for its pharmacological properties, including anti-oxidant, anti-inflammatory, and anti-cancer activities.
*Inflam↓,
AntiCan↓,
AntiAge↑, UA has potential as a key component in antiaging interventions.
chemoP↑, UA can counteract age-related muscle wasting and enhance physical performance, making it a valuable therapeutic for improving muscle health and combating sarcopenia
*neuroP↑, UA has neuroprotective properties because of its ability to reduce neuroinflammation, improve mitochondrial function, and mitigate oxidative stress,
*ROS↓,
*cognitive↑, suggesting its potential application in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and other age-related cognitive disorders)
*lipid-P↓, UA to reduce lipid peroxidation, combat oxidative stress, and improve endothelial function, promoting its role in cardiovascular health
*cardioP↑,
*TNF-α↓, exerts anti-inflammatory effects by suppressing the production of proinflammatory cytokines, such as TNF-α and IL-6, which can be employed for the management of chronic inflammatory conditions (such as rheumatoid arthritis and inflammatory bowel dise
*IL6↓,
GutMicro↑, Given that UA formation and bioactivity are influenced by the gut microbiota, its supplementation could promote a healthier gut microbiome, with potential therapeutic benefits for a wide range of conditions, including irritable bowel syndrome.
TumCCA↑, UA has potent anticancer effects through cell cycle arrest, apoptosis induction, and the modulation of oncogenic signaling pathways.
Apoptosis↑,
angioG↓, regulate the tumor microenvironment by inhibiting angiogenesis and inflammation
NF-kB↓, UA inhibited key signaling pathways, such as the NF-κB and PI3K/AKT pathways, which are critical for tumor progression
PI3K↓,
Akt↓,
Casp↑, UA also promoted apoptosis via the activation of caspases and the downregulation of survival proteins such as Survivin
survivin↓,
TumCP↓, inhibited MCF-7 cell proliferation in vitro and significantly reduced 27-HC-induced tumor growth in vivo.
cycD1/CCND1↓, UA induced cell cycle arrest by downregulating cyclin D1 and c-MYC and promoted apoptosis by increasing the expression of proapoptotic proteins such as Bax while reducing antiapoptotic BCL2 levels.
cMyc↑,
BAX↑,
Bcl-2↓,
COX2↓, UA, a metabolite of pomegranate mesocarp, synergistically reduced COX-2 expression by ~70% and increased cleaved caspase-3 levels
P53↑, UA induces the expression of tumor suppressor proteins such as p53 and p38-MAPK
p38↑,
*ROS↓, UA demonstrates significant antioxidant activity by reducing reactive oxygen species levels and enhancing the activities of key antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase.
*SOD↑,
*GPx↑,
SIRT1↑, UA induced cell cycle arrest and apoptosis while enhancing the expression of key tumor suppressors, including Sirtuin 1 (Sirt1) and Forkhead box protein O1 (FOXO1)
FOXO1↑,
eff↑, UA preferentially accumulates in prostate and intestinal tissues, suggesting its targeted bioactivity.
ChemoSen↑, UA has emerged as a potent chemosensitizing agent that enhances the efficacy of conventional cancer therapies.
Showing Research Papers: 1 to 40 of 40
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 40
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 16, ARE↑, 1, Catalase↑, 2, Ferroptosis↑, 1, GPx4↓, 1, GSH↓, 2, GSTs↑, 1, HO-1↓, 2, HO-1↑, 2, HO-2↓, 1, lipid-P↓, 1, MDA↓, 1, NRF2↓, 1, NRF2↑, 2, NRF2⇅, 1, ROS↓, 6, ROS↑, 17, ROS⇅, 2, ROS↝, 3, SOD↑, 2,
Metal & Cofactor Biology ⓘ
Ferritin↑, 1, FTH1↓, 1, NCOA4↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, MMP↓, 5, mtDam↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, cMyc↓, 1, cMyc↑, 1, ECAR↝, 1, GlucoseCon↓, 2, Glycolysis↓, 1, HK2↓, 1, lactateProd↓, 2, LDHA↓, 1, LDL↓, 1, NAD↑, 1, PDH↑, 1, PDK1?, 2, SIRT1↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 3, Akt↑, 1, p‑Akt↓, 3, Apoptosis↓, 2, Apoptosis↑, 7, Bak↑, 1, BAX↑, 5, Bax:Bcl2↑, 2, Bcl-2↓, 4, Bcl-xL↓, 1, Casp↑, 3, Casp12↑, 1, Casp3↓, 1, Casp3↑, 6, Casp9↑, 2, Cyt‑c↑, 4, Diablo↑, 2, Fas↑, 1, Ferroptosis↑, 1, hTERT/TERT↓, 1, iNOS↓, 2, JNK↑, 1, Mcl-1↓, 1, MDM2↓, 1, Myc↓, 1, NOXA↑, 1, p27↑, 4, p38↑, 1, PUMA↑, 1, survivin↓, 3, Telomerase↓, 1,
Kinase & Signal Transduction ⓘ
AMPKα↑, 1, p70S6↓, 1,
Transcription & Epigenetics ⓘ
cJun↓, 1, Matr↓, 1, other↑, 1, other↝, 3, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 2, GRP78/BiP↑, 1, HSP27↓, 1, HSP70/HSPA5↓, 1, HSP90↓, 1, IRE1↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↝, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1, DNAdam↑, 4, P53↑, 5, cl‑PARP↑, 3, SIRT6↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 3, CDK2↑, 1, CDK4↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 4, cycE/CCNE↓, 2, cycE/CCNE↑, 1, P21↑, 4, p‑RB1↓, 1, TumCCA↑, 9,
Proliferation, Differentiation & Cell State ⓘ
CDK8↓, 1, cFos↓, 1, cMET↓, 1, CSCs↓, 1, EMT↓, 2, EMT↑, 1, p‑ERK↓, 1, FOXO1↑, 1, HDAC↓, 1, mTOR↓, 3, p‑mTOR↓, 1, mTORC1↓, 1, NOTCH↓, 1, NOTCH1↓, 1, PI3K↓, 3, PTEN↑, 2, STAT3↓, 3, p‑STAT3↓, 1, TumCG↓, 5, Wnt/(β-catenin)↓, 1,
Migration ⓘ
AntiAg↑, 1, Ca+2↑, 1, Ca+2↝, 1, E-cadherin↑, 2, p‑FAK↓, 1, MMP2↓, 3, MMP9↓, 5, MMPs↓, 1, N-cadherin↓, 2, PKCδ↓, 1, SMAD3↓, 1, Snail↓, 1, TGF-β↓, 3, TJ↓, 1, Treg lymp↓, 1, TumCI↓, 3, TumCMig↓, 5, TumCP↓, 6, TumMeta↓, 3, Twist↓, 1, uPA↓, 1, Vim↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 6, ATF4↑, 1, EGFR↓, 1, Endoglin↑, 1, HIF-1↓, 1, Hif1a↓, 3, LOX1↓, 1, NO↑, 2, VEGF↓, 2,
Barriers & Transport ⓘ
GLUT1↓, 1, NHE1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 6, COX2↑, 1, CRP↓, 1, Igs↑, 1, IL10↑, 1, IL1β↓, 2, IL6↓, 1, Imm↑, 1, INF-γ↓, 1, Inflam↓, 6, Inflam↝, 1, JAK↓, 1, NF-kB↓, 5, NK cell↑, 1, PD-L1↓, 1, PGE2↓, 1, TNF-α↓, 3,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, ADAM10?, 1,
Protein Aggregation ⓘ
NLRP3↓, 1,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 3, ER(estro)↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 11, DDS↑, 1, Dose?, 1, Dose↑, 4, Dose↝, 4, Dose∅, 1, eff↓, 3, eff↑, 13, Half-Life↝, 2, RadioS↑, 5, selectivity↑, 4,
Clinical Biomarkers ⓘ
BP↓, 1, CRP↓, 1, E6↓, 1, E7↓, 1, EGFR↓, 1, Ferritin↑, 1, GutMicro↑, 1, hTERT/TERT↓, 1, IL6↓, 1, Myc↓, 1, PD-L1↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiCan↓, 1, AntiCan↑, 7, cardioP↑, 1, chemoP↑, 3, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 2, radioP↑, 1, Risk↓, 4, toxicity↓, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 218
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 24, antiOx↑, 1, Catalase↑, 2, GPx↑, 4, GSH↑, 8, GSR↑, 1, H2O2↓, 1, HDL↑, 1, HNE↓, 1, HO-1↑, 2, lipid-P↓, 3, MDA↓, 4, MPO↓, 1, NRF2↑, 4, ROS↓, 11, ROS↑, 1, SOD↑, 6, VitC↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, mitResp↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
12LOX↓, 1, adiP↓, 1, ALDOA↑, 1, p‑cMyc↑, 1, CRM↑, 1, GPI↑, 1, HK2↑, 1, LDH↓, 1, LDHA↑, 1, LDL↓, 1, NAD↑, 1, PFKL↑, 1, PKM1↑, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↓, 1, Casp3↓, 1, Casp7↓, 1, Fas↓, 1, iNOS↓, 3, iNOS↑, 1, MAPK↓, 2, Telomerase↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1, other↑, 1,
Protein Folding & ER Stress ⓘ
CHOP↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1,
DNA Damage & Repair ⓘ
PCNA↓, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, PI3K↓, 1, STAT3?, 1,
Migration ⓘ
APP↓, 1, CLDN1↑, 1, MUC1↑, 1, ZO-1↑, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 2, NO↑, 1,
Barriers & Transport ⓘ
BBB↓, 1, CLDN3↑, 1, IBI↑, 1, OCLN↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CRP↓, 1, IFN-γ↓, 1, IL1β↓, 2, IL6↓, 3, Imm↑, 2, Inflam↓, 17, JAK2↑, 1, NF-kB↓, 2, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 3,
Synaptic & Neurotransmission ⓘ
AChE↓, 2, BChE↓, 1, MAOA↓, 2, p‑tau↓, 2,
Protein Aggregation ⓘ
Aβ↓, 2, BACE↓, 1, MAOB↓, 1, NLRP3↓, 3,
Drug Metabolism & Resistance ⓘ
BioAv↓, 5, BioAv↑, 4, BioAv↝, 1, Dose↝, 1, eff↓, 3, eff↑, 1, eff↝, 1, Half-Life↓, 1, Half-Life↑, 2,
Clinical Biomarkers ⓘ
BG↓, 1, CRP↓, 1, GutMicro↑, 3, GutMicro↝, 1, IL6↓, 3, LDH↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, AntiDiabetic↑, 1, BOLD↑, 1, cardioP↑, 4, cognitive↑, 4, hepatoP↑, 5, memory↑, 5, motorD↑, 1, neuroP↑, 9, Pain↓, 1, Risk↓, 5, toxicity∅, 2,
Infection & Microbiome ⓘ
Bacteria↓, 2,
Total Targets: 110
Scientific Paper Hit Count for: antiOx, anti-oxidant activities
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#:1103 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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