hepatoP Cancer Research Results
hepatoP, L,hepatoprotective: Click to Expand ⟱
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Hepatoprotective is the ability of a chemical substance to prevent damage to the liver.
Grapefruit:
-hepatoprotective potential has emerged from the study of naringenin and naringin.
Blueberries/cranberries:
-proanthocyanidins
Grape:
Nopal (Cactus pear) and tuna (Cactus pear fruit) “Opuntia ficus-indica”:
Chamomile (Matricaria chamomilla or Chamomilla recutita):
Silymarin (Silybum marianum):
Blue green algae spirulina :
Propolis (bee glue):
POLYSACCHARIDES
β-glucans
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Scientific Papers found: Click to Expand⟱
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in-vivo, |
Liver, |
HepG2 |
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*hepatoP↑, histopathological studies indicated that the liver acrylamide induced in mice showed
necrosis and damage in liver cells, but the treatment of mice with SeNPs, reduced the effect of
acrylamide significantly.
AntiCan↑, green synthesized SeNPs exhibit both in vitro and in vivo
anticancer and hepatoprotective effects
*hepatoP↑, silver nanoparticles were effective in protecting the liver from damages induced by carbon tetrachloride
*LDH↓, LDH is a prominent indicator and a diagnostic tool for tissue injury.45 LDH levels were elevated in the control group, but were effectively restored to normal in groups treated with test (AgNPs)
hepatoP↑, Treatment with crude extract and silver nanoparticles of Cucumis melo fruit indicates that Cucumis melo fruit could have exerted its protective effect.
AST↓, AST ALT, ALP, LDH, GGT
ALAT↓,
ALP↓,
IL6↓, diminish the levels of inflammatory markers (IL-6, TNF-α, and IL-1β) via NF-κB pathway
TNF-α↓,
IL1β↓,
hepatoP↑, CCAgNPs significantly down-regulated the serum marker enzymes of hepatic and non-hepatic parameter, elevated the levels of enzymatic and non-enzymatic antioxidant profile, elevation in membrane bound enzymes
hepatoP↑, AgNPs may be considered as a therapeutic agent for liver related malignancies.
CD44↓,
CSCs↓, in DEN + AgNPs and AgNPs groups it were similar to control group
hepatoP↑, hepatoprotective activity of silver nanoparticles (AgNPs) synthesized using aqueous extracts of Andrographis paniculata leaves (ApAgNPs) and Semecarpus anacardium nuts (SaAgNPs) against diethylnitrosamine (DEN) induced liver cancer in mice model
*AST↓, decreased level of aspartate amino transferase (AST), alanine amino transferase (ALT), serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT) activity
*ALAT↓,
*Catalase↑, and elevated level of catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activity
*GPx↑,
*GSTA1↑,
*SOD↑,
TumCD↑, IC50 values of the AgNPs, AuNPs and Ag/AuNPs on HepG2 cells were determined as 38.42 μg ml-1, 43.25 μg ml-1 and 39.20 μg ml-1
TumVol↓, tumour reduction (∼45 to 65%) was observed in the nanoparticle-treated animal
*toxicity↝, The No-Observed-Adverse-Effect-Level (NOAEL) for the AgNPs was determined to be 2000 mg per kg of body weight (bw) from an acute toxicity test.
hepatoP↑, (Ag/AuNPs) for hepatoprotective activity against diethylnitrosamine (DEN)-induced liver cancer in a Sprague Dawley (SD) rat model
*eff↑, Treatment with AgNPs led to a notable reduction in damages of liver, kidney, lung, stomach and duodenum.
*RenoP↑,
*hepatoP↑,
*MDA↓, AgNPs treated groups reduced the levels of tissues MDA and increased the levels of tissues SOD and GSH.
*SOD↑,
*GSH↑,
*TNF-α↓, The expression levels of TNF-α mRNA and IL-1β mRNA were reduced in the rats treated by silver nanoparticles.
*IL1β↓,
*hepatoP↑, AgNPs + RV treatment significantly reduced pro-inflammatory cytokines, NF-κB activation, presepsin, PCT, 8-OHDG, and VEGF levels compared with the CLP group, indicating attenuation of sepsis-induced liver injury.
*Inflam↓,
*NF-kB↓,
*VEGF↓,
*SIRT1↑, Both RV and AgNPs + RV treatments increased SIRT1 levels, suggesting a potential role of SIRT1 activation in mediating the protective effects.
*ROS↓, alleviating sepsis-induced liver injury by modulating inflammation, oxidative stress, and endothelial dysfunction, potentially mediated through SIRT1 activation.
*Dose↝, 30 mg/kg of AgNPs + RV was given intraperitoneally to the rats
*Catalase↑, AgNPs + RV treatment exhibited a robust effect in bolstering CAT activity
*MDA↓, AgNPs + RV treatment effectively ameliorates sepsis-induced oxidative stress and inflammation in rat livers by reducing MDA, MPO, and NO levels
*MPO↓,
*NO↓,
*ALAT↓, AgNPs + RV effectively reduced the ALT and AST levels, returning them to values similar to those observed in the Sham group
*AST↓,
*antiOx↑, corroborates the antioxidant potential of RV and AgNPs observed in earlier studies
*Dose↝, The treated group received a single oral dose of 5.5 mg/kg of Ag NPs. 5 to 12 nm
*eff↑, Ag NPs treatment in septic mice significantly decreased liver enzyme activities, total protein, and serum albumin.
*RenoP↑, Ag NPs significantly enhanced kidney function, as indicated by a significant decrease in the levels of creatinine, urea, and uric acid.
*antiOx↑, Ag NPs showed a powerful antioxidant effect via the considerable reduction of malondialdehyde and nitric oxide levels and the increase in antioxidant content.
*MDA↓,
*NO↓,
*hepatoP↑, hepatoprotective effect of Ag NPs may be attributed to their antioxidant properties
*toxicity↝, The Ag NPs dose is 1/10 of LD50, which is 5.5 mg/kg.
*GSH↑, GSH, SOD, GST, and CAT of the septic group. Meanwhile, the Ag NPs-treated mice showed a significant (p < 0.05) increase in all four parameters.
*SOD↑,
*GSTs↑,
*Catalase↑,
*BioAv↑, another key property of allicin is its hydrophobicity, which allows it to be absorbed easily through the cell membrane without causing any physical or chemical damage to the phospholipid bilayer, thereby allowing its rapid metabolism to produce pharm
*cardioP↑, Allicin exhibits protective effects in multiple organ systems, including the brain, intestines, lungs, liver, kidneys, prostate, and heart.
*hepatoP↑,
*RenoP↑,
*Half-Life↝, half-life (t1/2)of allicin was 227 min–260 min. Because allicin is eliminated from the body by the respiratory tract, the concentration of allicin in lung tissue is significantly lower than that in the blood
*BioAv↓, We believe that the bioavailability of allicin is relatively low for the following reasons: At first, allicin is characterized by a distinctive garlic odor and chemical instability. It can be easily degraded under room temperature.
*neuroP↑, Neuroprotective activity
*cognitive↑, On the other hand, allicin improves cognitive deficits via Protein kinase R-like endoplasmic reticulum kinase (PERK)/Nuclear factor erythroid-2-related factor 2 (NRF2) signaling pathway and c-Jun N-terminal kinase (JNK) signaling pathways
*ROS↓, They found that allicin suppressed ROS generation and decreased lipid peroxidation in 6-hydroxydopamine (6-OHDA)-induced Pheochromocytoma 12 (PC12) cells
*lipid-P↓,
*DNArepair↑, Allicin not only directly protects DNA, but also indirectly protects DNA through antioxidant activity and regulation of oxidizing enzymes
*ChemoSen↑, Allicin combined with other chemotherapy drugs showed a better anti-cancer effect
*antiOx↑, The significant functional act of garlic is its anticancer, antimicrobial, antioxidant, antidiabetic, antifibrinolytic, immune enhancing, antiplatelet collected effect and its possible act in prohibiting cardiovascular illnesses
*AntiAg↑,
*cardioP↑,
Ca+2↑, Sultan et al.[34] stated that allicin is cytotoxic to monocytic leukemia cells (THP-1 cells) and stimulates calcium-linked hemolysis and eryptosis in human red blood cells. Allicin advances calcium grades in cells, reasons to oxidative stress and al
ROS↑, Allicin advances calcium grades in cells, reasons to oxidative stress and also induces CK1a, caspase, p38, mitogen-activated protein kinase
Casp↑,
p38↑,
MAPK↑,
hepatoP↑, Wu et al.[42] clarified that allicin applies hepaprotective action counter to hepatic toxicity of cells
chemoP↑, Throughout with other garlic preparations, aged garlic extract (AGE) has been indicated to have hepatoprotective, immune, improving, anticancer, and chemoprotective actions.
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Park, |
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*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,
AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,
*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in
acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits
the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models
*hepatoP↑, Curc and Lip acid can be considered as promising natural therapies against liver injury, induced by NHPA, through their antioxidant and antifibrotic actions.
*α-SMA↓, Curc and Lip acid reduced the expression of alpha-smooth muscle actin and collagen III, upregulated by NHPA intoxication
*COL3A1↓,
*ROS↓, scavenging activity to ROS and a capacity to regenerate endogenous antioxidants such as GSH, and vitamins C and E.
*GSH↑,
*ALAT↓, ALT, AST, and ALP activity levels compared to those of the control group. The use of NACS, Curc, and/or Lip acid significantly reduced the toxic effects of NHPA on those enzymes,
*AST↓,
*ALP↓,
*MDA↓, The combination therapy showed an apparent reduction in MDA level more than other treatments
*AntiCan↑, clinical studies are beginning to affirm apigenin's therapeutic benefits, showing positive effects in treating cancer, cardiovascular diseases, diabetes, neurodegenerative disorders, and inflammatory conditions.
*cardioP↑, The findings suggest that apigenin could serve as an effective therapeutic agent to reduce cardiotoxicity caused by Doxorubicin
*neuroP↑,
*Inflam↓,
*antiOx↑, apigenin (5,7,4′-trihydroxyflavone) is a flavonoid that chelates redox-active metals and has antioxidant properties
*hepatoP↑, Overall, the results indicate that apigenin alleviated liver injury by reducing inflammation and oxidative stress via suppression of the non-canonical NF-κB pathway
ChemoSen↑, Apigenin increases the cytotoxicity of sorafenib
*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,
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NRK52E |
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*RenoP↑, WFA ameliorated renal damage, improved kidney function, and decreased levels of creatinine, BUN, UA, and XOD in PO-induced hyperuricemic mice.
*hepatoP↑,
*creat↓,
*BUN↓,
*uricA↓,
*Apoptosis↓, WFA markedly inhibited renal apoptosis, accompanied by changes of apoptosis-related proteins.
*α-SMA↓, Notably reduced α-SMA expression was observed after WFA administration, with WFA 10 mg/kg group presenting the most significant inhibitory effect.
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HCC, |
HepG2 |
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NF-kB↓, We found that many of Nuclear factor kappa B (NF-κB), angiogenesis and inflammation associated proteins secretion is downregulated upon Withaferin A treatment.
angioG↓,
Inflam↓,
TumCP↓, uppressed the proliferation, migration, invasion, and anchorage-independent growth of these HCC cells.
TumCMig↓,
TumCI↓,
Sp1/3/4↓, Withaferin A inhibits NF-κB, Specificity protein 1 (Sp1) transcription factors, and downregulates Vascular Endothelial Growth Factor (VEGF) gene expression
VEGF↓,
angioG↓, Withaferin A (2.5 µM) treatment decreased the secretion of various angiogenesis-related markers, growth factors, and cytokines (Serpin F1(PEDF), uPA, PDGF-AA, Angiogenin, Endothelin-1, Macrophage migration inhibitory factor (MIF), PAI-1, MCP1, ICAM-1
uPA↓,
PDGF↓,
MCP1↓,
ICAM-1↓,
*NRF2↑, It also upregulates the Nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor and protects from Acetaminophen-induced hepatotoxicity and liver injury
*hepatoP↑,
MAPK↑, Figure 3
p38↑,
BAX↑,
BIM↑,
CHOP↑,
ROS↑,
DR5↑,
Apoptosis↑,
Ferroptosis↑,
GPx4↓,
BioAv↝, WA has a rapid oral absorption and reaches to peak plasma concentration of around 16.69 ± 4.02 ng/ml within 10 min after oral administration of Withania somnifera aqueous extract at dose of 1000 mg/kg, which is equivalent to 0.458 mg/kg of WA
HSP90↓, table 1 10uM) were found to inhibit the chaperone activity of HSP90
RET↓,
E6↓,
E7↓,
Akt↓,
cMET↓,
Glycolysis↓, by suppressing the glycolysis and tricarboxylic (TCA) cycle
TCA↓,
NOTCH1↓,
STAT3↓,
AP-1↓,
PI3K↓,
eIF2α↓,
HO-1↑,
TumCCA↑, WA (1--3 uM) have been reported to inhibit cell proliferation by inducing G2 and M phase cycle arrest inovarian, breast, prostate, gastric and myelodysplastic/leukemic cancer cells and osteosarcoma
CDK1↓, WA is able to decrease the cyclin-dependent kinase 1 (Cdk1) activity and prevent Cdk1/cyclin B1 complex formation, which are key steps in cell cycle progression
*hepatoP↑, A treatment (40 mg/kg) reduces acetaminophen-induced liver injury (AILI) in mouse models and decreases H 2O 2-induced glutathione (GSH) depletion and necrosis in hepatocyte
*GSH↑,
*NRF2↑, WA triggers an anti-oxidant response after acetaminophen overdose by enhancing hepatic transcription of the nuclear factor erythroid 2ârelated factor 2 (NRF2)-responsive gene
Wnt↓, indirectly inhibit Wnt
EMT↓, WA can also block tumor metastasis through reduced expression of epithelial mesenchymal transition (EMT) markers.
uPA↓, WA (700 nM) exert anti-meta-static activities in breast cancer cells through inhibition of the urokinase-type plasminogen activator (uPA) protease
CSCs↓, s WA (125-500 nM) suppress tumor sphere formation indicating that the self-renewal of CSC is abolished
Nanog↓, loss of these CSC-specific characteristics is reflected in the loss of typical stem cell markers such as ALDH1A, Nanog, Sox2, CD44
and CD24
SOX2↓,
CD44↓,
lactateProd↓, drop in lactate levels compared to control mice.
Iron↑, Furthermore, we found that WA elevates the levels of intracellular labile ferrous iron (Fe +2 )
through excessive activation of heme oxygenase-1 (HMOX1), which independently causes accumulation of toxic lipid radicals and ensuing ferroptosis
NF-kB↓, nhibition of NF-kB kinase signaling pathway
*hepatoP↑, Withania Somnifera, is a hepatoprotective agent
*IKKα↓, WA also inhibits inflammation by directly inhibiting IκκB activity46,47 or NLRP3 inflammasome activation in vitro in immune cells
*NLRP3↓,
*NRF2↑, WA probably protects against FH by targeting the macrophage and/or hepatocyte stress via activating NRF2, AMPKα
*AMPK↑,
*Inflam↓, Thus, WA potently protects against GalN/LPS-induced hepatotoxicity and inflammation
*Apoptosis↓, WA suppressed hepatic apoptosis in vivo
*cl‑Casp3↓, attenuate the increase of cleaved CASP3 and cleaved PARP1
*cl‑PARP1↓,
*NLRP3↓, WA prevented GalN/LPS-induced FH partially by inhibiting activation of the NLRP3 inflammasome
*ROS↓, fig 7
*ALAT↓,
*AST↓,
*GSH↑, (GSH) levels were significantly depleted by ~50% 6 h after GalN/LPS administration and were recovered to levels comparable with that of control mice by WA treatment
AntiCan↑, assess the anticancer effect of melatonin (MEL) and ascorbyl palmitate-loaded pluronic nanoparticles (APnp) combination on Ehrlich ascites carcinoma
(EAC)-bearing mice.
TumCG↓, MEL alone showed a decrease in tumor growth by 48%, while in the case of using MEL combined with APnp, it displayed inhibition of tumor growth by 62%
Apoptosis↑, It also induced apoptosis and DNA damage.
DNAdam↑,
TumCCA↑, Besides, mediated cell cycle arrest.
IL6↓, IL-6/STAT3
pathway was inactivated to a greater extent after our combination treatment.
STAT3↓,
TumCP↓, antiproliferative effect of MEL and APnp via decreased expression of Ki-67
Ki-67↓,
TumCI↓, Our combination of MEL and APnp was able to inhibit cancer cell invasion and metastasis by decreasing the protein expression of MMP-9.
TumMeta↓,
MMP9↓,
eff↑, The synergy score was 21.06 ( > 10 indicates synergistic effect)
*Catalase↑, Administration of MEL alone or MEL+ APnp treated mice showed a significant and highly significant increase, respectively (P<0.05, P<0.01) in the antioxidant enzyme activities of CAT and SOD, and GSH.
*SOD↑,
*GSH↑,
*MDA↓, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control
group.
*NO↓,
*antiOx↑, Figure 2 demonstrated a highly significant and extremely significant reduction,
respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control
group.
*hepatoP↑, combined MEL and
APnp- treated animals displayed a noteworthy amelioration for all examined organs when
compared to the control EAC inoculated group, Figure 3.
*RenoP↑,
Apoptosis↑, Astaxanthin causes apoptosis in
several in vitro studies, including both oral and liver cancer cells
EMT↓, AXT inhibits the EMT pathway in colon cancer cells and can reduce breast cancer cells' proliferation and growth
AntiCan↑, Astaxanthin can address human health problems, including cancer, cardiovascular, and neurodegenerative diseases.
*cardioP↑,
*neuroP↑,
TumCG↓, 100 mg/kg Astaxanthin strongly inhibited tumor growth relative to the TC group, with an inhibitory rate of 41.7%.
*antiOx↑, .ASX is often referred to as the "super antioxidant" since it has the strongest antioxidant activity of current carotenoids.
*Bacteria↓, Studies have demonstrated antioxidant and antimicrobial, immunomodulatory, hepatoprotective, anticancer, and antidiabetic effects of ASX.
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
ROS↓, Astaxanthin and carbendazim function in conjunction to inhibit cell proliferation while reducing ROS production in
breast cancer cells.
*chemoPv↑, Chemopreventive and therapeutic efficacy of astaxanthin against cancer
*AST↓, The in vivo results showed that HS15-BA micelles significantly inhibited the activity of the CCl4-induced liver injury marker enzymes aspartate transaminase (AST) and alanine transaminase (ALT).
*ALAT↓,
*GSH↓, leading to increased L-glutathione (GSH) and superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) activity, while HS15-BA significantly reversed the above changes.
*SOD↓,
*MDA↓,
*hepatoP↑, BA also had a hepatoprotective effect through anti-inflammatory activity;
*Inflam↓,
BioAv↑, In summary, our study confirmed that HS15-BA micelles enhanced the bioavailability of BA, and showed hepatoprotective effects through antioxidant and anti-inflammatory activities.
*AntiCan↑, antibacterial, antiviral, anticancer, anticonvulsant, anti-oxidant, hepatoprotective, and neuroprotective effects.
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*ROS↓, pharmacological properties of baicalin and baicalein are due to their abilities to scavenge reactive oxygen species (ROS)
Ca+2↑, Baicalein mainly induced apoptosis through Ca+2 influx via Ca2+ release from the reticulum to cytosol dependent on phospholipase C protein
ROS↑, ROS production is associated with baicalein-induced apoptosis via Ca2+-dependent apoptosis in tongue and breast cancer cells (78, 79)
BAX↑, The level of Bax/Bcl-2 increased and caspase-3 and -9 were activated following the release of cytochrome C (80).
Casp3↑,
Casp9↑,
Cyt‑c↑,
MMP↓, In gastric cancer cells, baicalein mediated apoptosis in a dose-dependent manner through disruption of mitochondrial membrane potential
Mcl-1↓, In pancreatic cancer cells, baicalein induced apoptosis via suppression of the Mcl-1 protein.
PI3K↓, In HepG2 cells, baicalin-copper induced apoptosis through down-regulation of phosphoinositide-3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway
Akt↓,
mTOR↓,
BAD↓, Studies demonstrated that baicalein treatment suppressed Bad, ERK1/2 phosphorylation, and MEK1 expression both in vitro and in vivo.
ERK↓,
MEK↓,
DR5↑, Baicalein enhanced the activity of death receptor-5 (DR5) in prostate cancer PC3 cells.
Fas↑, baicalin is the active ingredient that acts as Fas ligand and caused up-regulation of Fas protein (89).
TumMeta↓, Baicalin/baicalein not only induced apoptosis in cancer cells but also suppressed metastasis.
EMT↓, both baicalin and baicalein inhibited epithelial-mesenchymal transition (EMT) through the suppression of TGF-β in breast epithelial cells through the NF-κB pathway (92).
SMAD4↓, baicalein suppressed metastasis in gastric cancer through inactivation of the Smad4/TGF-β pathway (93).
TGF-β↓,
MMP9↓, baicalin and baicalein inhibition of the expression level of matrix metalloproteinases (MMP) such as MMP-9 and MMP-2 in liver, breast, lung, ovarian, gastric, and colorectal cancers and glioma
MMP2↓,
HIF-1↓, Baicalin attenuated lung metastasis through inhibition of hypoxia-inducible factor (HIF)
12LOX↓, Baicalein acts as an anticancer agent via inhibiting 12-lipooxygenase (12-LOX),
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toxicity↝, We have found that baicalin and baicalein demonstrated cytotoxicity towards both cell lines, with more potent effects observed in baicalein.
ChemoSen↑, Both flavonoids, baicalin (167 µmol/L) and baicalein (95 µmol/L), synergistically enhanced the cytotoxic, proapoptotic, and genotoxic activity of doxorubicin and docetaxel in breast cancer cells.
selectivity↑, Surprisingly, low concentrations of baicalin and baicalein had a greater effect on MCF-7 viability. A
Apoptosis↑, Induction of Apoptosis and Necrosis by Baicalin and Baicalein Used alone and in Combination with Anticancer Drugs
necrosis↑,
MMP↓, After treatment with baicalin and baicalein at high concentrations (IC50), the ΔΨm of cancer cells was diminished to 30% of the control value
DNAdam↑, DNA Damage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
cl‑PARP↑, PARP Cleavage Induced by Baicalin and Baicalein Used Alone and in Combination with Anticancer Drugs
MRP1↓, Moreover, baicalin and baicalein reduced cisplatin resistance by inhibiting the expression of genes involved in drug resistance, such as MRP1 [30] and Bcl-2, and via the Akt/mTOR and Nrf2/Keap 1 pathway [26].
Bcl-2↓,
hepatoP↑, baicalin and baicalein can also help decrease the side effects of cisplatin treatment by protecting the liver from damage [31]
cardioP↑, Similar to baicalein, baicalin also significantly protects against doxorubicin’s cardiotoxicity.
BioAv↝, This is because baicalein has a smaller size and high lipophilicity, contributing to fast absorption and an improved ability to penetrate cells [60].
*TNF-α↑, elevated the serum level of TNF-α and IL-6 at the early phase, which indicated that baicalein could facilitate the initiating events in liver regeneration.
*IL6↑,
*hepatoP↑,
*hepatoP↑, baicalein's hepatoprotective action against different toxicity models (acetaminophen, cisplatin, doxorubicin, CCL4, monocrotaline, & d-galactosamine).
*neuroP↑, key pharmacological activities of baicalein against neurotoxicity (6-OHDA, rotenone, d-galactose, stroke, alzheimer, & sclerosis),
*Inflam↓, inflammation (arthritis, pulmonary fibrosis, & LPS-induced sepsis
*BioEnh↑, baicalein significantly increased the area under the curve (AUC) and Cmax of silybin and its conjugates, suggesting enhanced absorption in vivo.
*hepatoP↑, Moreover, coadministration of silybin with baicalein boosted the liver protective, antioxidant, and anti-inflammatory effects of silybin
*antiOx↑,
*Inflam↓,
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cardioP↑, cardioprotective activities.
Inflam↓, Decreasing the accumulation of inflammatory mediators and improving cognitive function
cognitive↑,
*hepatoP↑, Decreasing inflammation, reducing oxidative stress, regulating the metabolism of lipids, and decreasing fibrosis, apoptosis, and steatosis are their main hepatoprotective mechanisms
*ROS?, Reducing oxidative stress and protecting the mitochondria to inhibit apoptosis are proposed as hepatoprotective mechanisms of baicalin in NAFLD
*SOD↑, Baicalin could reduce the levels of ROS and fatty acid-induced MDA, and increase superoxide dismutase (SOD) and glutathione amounts compared to the control.
*GSH↑,
*MMP↑, Moreover, baicalin could partially restore mitochondrial morphology and increase ATP5A expression and mitochondrial membrane potential (Gao et al., 2022).
*GutMicro↑, After baicalein treatment, a remodelling in the overall structure of the gut microbiota was observed
ChemoSen↑, Besides, a combination of baicalin and doxorubicin could elevate the chemosensitivity of MCF-7 and MDA-MB-231 breast cancer cells
*TNF-α↓, Baicalin can protect cardiomyocytes from hypoxia/reoxygenation injury by elevating the SOD activity and anti-inflammatory responses through reducing TNF-α, enhancing IL-10 levels, decreasing IL-6, and inhibiting the translocation of NF-κB to the nucl
*IL10↑,
*IL6↓,
*eff↑, Studies show that baicalin and baicalein may be effective against IBD by suppressing oxidative stress and inflammation, and regulating the immune system.
*ROS↓,
*COX2↓, baicalein can improve the symptoms of ulcerative colitis by lowering the expression of pregnane X receptor (PXR), (iNOS), (COX-2), and caudal-type homeobox 2 (Cdx2), as well as the NF-κβ and STAT3
*NF-kB↓,
*STAT3↓,
*PGE2↓, Administration of baicalin (30-90 mg/kg) could decrease the levels of prostaglandin E2 (PEG2), myeloperoxidase (MPO), IL-1β, TNF-α, and the apoptosis-related genes including Bcl-2 and caspase-9
*MPO↓,
*IL1β↓,
*MMP2↓, Rheumatoid arthritis RA mouse model by supressing relevant proinflammatory cytokines such as IL-1b, IL-6, MMP-2, MMP-9, TNF-α, iNOS, and COX-2)
*MMP9↓,
*β-Amyloid↓, Alzheimer’s disease (AD) : reduce β-amyloid and trigger non-amyloidogenic amyloid precursor proteins.
*neuroP↑, For instance, administration of baicalin orally for 14 days (100 mg/kg body weight) exhibited neuroprotective effects on pathological changes and behavioral deficits of Aβ 1–42 protein-induced AD in vivo.
*Dose↝, administration of baicalin (500 mg/day, orally for 12 weeks) could improve the levels of total cholesterol, TGs, LDLC and apolipoproteins (APOs), and high-sensitivity C-reactive protein (hs-CRP) in patients with rheumatoid arthritis and coronary arte
*BioAv↝, the total absorption of baicalin depends on the activity of intestinal bacteria to convert baicalin to baicalein as the first step.
*BioAv↝, Kidneys, liver, and lungs are the main organs in which baicalin accumulates the most.
*BBB↑, Baicalin and baicalein can pass through the blood brain barrier (BBB)
*BDNF↑, mechanism of action for baicalein is illustrated in Figure 3. Activation of the BDNF/TrkB/CREB pathway, inhibition of NLRP3/Caspase-1/GSDMD pathway,
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AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,
*toxicity↓, These flavonoids have almost no toxicity to human normal epithelial, peripheral and myeloid cells
*antiOx↑, antioxidant and anti-inflammatory activities are largely due to their abilities to scavenge the reactive oxygen species (ROS)
*Inflam↓,
*ROS↓,
*NF-kB↓, by attenuating the activity of NF-κB and suppressing the expression of several inflammatory cytokines and chemokines including monocyte chemotactic protein-1 (MCP-1)
*MCP1↓,
*hepatoP↑, Both baicalin and baicalein ... including antioxidant, anti-inflammatory, anticancer, anticardiovascular, antidiabetic, hepatoprotective, antiviral, anti-ulcerative colitis, antithrombotic, eye protective and neuroprotective activities
*neuroP↑,
*hepatoP↑, baicalein significantly ameliorated APAP-exposed liver damage and histological hepatocyte changes
*MDA↓, baicalein (50 or 100 mg/kg) pretreatment significantly inhibited liver MDA level (p < 0.05; Figure 4), increased SOD, CAT and GSH activity.
*SOD↑,
*Catalase↑,
*GSH↑,
*MAPK↓, Baicalein Prevented the MAPK Pathway Activation
*p‑JAK2↓, BAI Suppressed the Expression of p-JAK2 and p-STAT3 Proteins in APAP Liver Injury
*p‑STAT3↓,
*ALAT↓, our experimental results suggested that serum ALT and AST levels were obviously alleviated by Baicalein in a dose-dependent manner
*AST↓,
*ROS↓, hepatoprotective role of BAI via attenuating oxidative stress
*antiOx↑, hepatoprotective activity of Baicalein might be associated with its antioxidative capacity.
*Inflam↓, including anti-inflammatory, antioxidative, anti-apoptotic, antiproliferative, and antihypertensive.
*antiOx↑,
*ER Stress↓, BBR can decrease apoptosis and inflammation following different pathological conditions, which might be mediated by targeting ER stress pathways.
*cardioP↑, protective potential of BBR against several diseases, such as metabolic disorders, cancer, intestinal diseases, cardiovascular, liver, kidney, and central nervous system diseases, in both in vivo and in vitro studies.
*RenoP↑,
*hepatoP↑,
*hepatoP↑, berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM)
*LC3II↑, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats.
*Beclin-1↑,
*AMPK↑,
*mTOR↑,
*ER Stress↓, It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation.
*CHOP↓,
*JNK↓,
*ROS↓,
*Inflam↓,
*BG↓, Oral supplementation of diabetic rats either by Lip-BBR or Vild, 10 mg/kg of each, significantly (p < 0.001) lowered the blood glucose levels of tested diabetic rats compared to the diabetic group.
*SOD↑, when the diabetic rats received Lip-BBR, the decrements were less pronounced compared to the diabetic group by 1.16 fold, 2.52 fold, and 67.57% for SOD, GPX, and CAT, respectively.
*GPx↑,
*Catalase↑,
*IL10↑, Treatment of the diabetic rats with Lip-BBR significantly (p < 0.001) elevated serum IL-10 levels by 37.01% compared with diabetic rats.
*IL6↓, Oral supplementation of Lip-BBR could markedly (p < 0.0001) reduce the elevated serum levels of IL-6 and TNF-α when it is used as a single treatment by 55.83% and 49.54%,
*TNF-α↓,
*ALAT↓, ALT, AST, and ALP in the diabetic group were significantly higher (p < 0.0001) by 88.95%, 81.64%, and 1.8 fold, respectively, compared with those in the control group, but this was reversed by the treatment with Lip-BBR
*AST↓,
*ALP↓,
*antiOx↑, Berberine has multiple therapeutic actions, including antioxidant, anti‐inflammatory, antitumour, antimicrobial, hepatoprotective, hypolipidemic, and hypoglycemic actions.
*Inflam↓,
*hepatoP↑,
*eff↑, recent studies show that berberine has a protective effect on central nervous system disorders, such as Alzheimer's, cerebral ischaemia, mental depression, schizophrenia, and anxiety
*5HT↑, Chronic administration of berberine (5 mg/kg, ip) for 15 days significantly increased the levels of norepinephrine (29%), serotonin (19%) as well as dopamine (52%)
*Mood↑, An antidepressant effect of berberine results from elevation of brain‐derived neurotrophic factor (BDNF) levels.
*BDNF↑,
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*AntiDiabetic↑, Through modulating oxidative stress, SIRT-1 expression, PPAR gamma receptors, and other multiple mechanisms biochanin-A produces anti-diabetic action.
*neuroP↑, Biochanin-A has been shown to have a potential neuroprotective impact by modulating multiple critical neurological pathways.
*toxicity↓, Unlike chemical agents such as chemotherapeutic agents, isoflavones have shown zero toxicity to humans
*CYP19↓, Biochanin-A inhibits CYP19 and negatively affects the synthesis of oestrogen in the body which enhances the anti-oestrogenic property in hormone-influenced cancer such as prostate cancer and breast cancer
p‑Akt↓, Biochanin-A inhibits Akt phosphorylation thereby downregulates mTOR signals and disrupts the cell cycle.
mTOR↓,
TumCCA↑,
P21↑, Biochanin-A cause apoptosis in lung cancer by increasing p21, caspase-3, and Bcl-2 levels. It lowers E-cadherin and blocks metastasis.
Casp3↑,
Bcl-2↑,
Apoptosis↑,
E-cadherin↓,
TumMeta↓,
eff↑, The synergism of biochanin-A with 5-fluorouracil evidenced in Caco-2 and HCT-116 cell lines indicates the modulatory influence of biochanin-A in colon cancer treatment.
GSK‐3β↓, It blocked the “Akt and GSK3β phosphorylation and boosted the degradation of β-catenin” ( Mahmoud et al., 2017).
β-catenin/ZEB1↓,
RadioS↑, Biochanin-A when combined with gamma radiation on HT29 cells, which is resistant to radiation, had revealed a reduction in cell proliferation.
ROS↑, Raised levels of ROS, lipid peroxidation, MMP, caspase-3 have been observed more in the treatment group with significant apoptosis
Casp1↑,
MMP2↓, biochanin-A influenced the tumour invasion capacity by lowering matrix-degrading enzymes (MMP 2 and MMP 9) tested in U87MG cells
MMP9↓,
EGFR↓, Biochanin-A by lowering EGFR, p-ERK (Extracellular signal related kinases), p-AKT (Protein kinase-B), c-myc, and MT-MMP1 (Membrane type matrix metalloproteinase) activation, inhibited cell survival.
ChemoSen↑, Biochanin-A synergistically improved temozolomide anti-cancer ability in GBM
PI3K↓, Cell signalling pathways MAP kinase, PI3 kinase, mTOR, matrix metalloproteases, hypoxia-inducible factor, and VEGF were inhibited by biochanin-A, making it suitable in treating GBM
MMPs↓,
Hif1a↓,
VEGF↓,
*ROS↓, anti-diabetic mechanism of biochanin-A is by decreasing oxidative stress
*Obesity↓, strongly suggest that biochanin-A has therapeutic potential in the treatment of obesity and the prevention of cardiovascular disease
*cardioP↑,
*NRF2↑, Biochanin-A up-regulated the Nrf-2 pathway while suppressing the NF-κB cascade,
*NF-kB↓, By activating the Nrf-2 pathway and inhibiting NF-κB activation, biochanin-A may reduce obesity and its related cardiomyopathy by decreasing oxidative stress and inflammation
*Inflam↓,
*lipid-P↓, cardio-protective effects by controlling lipid peroxidation
*hepatoP↑, biochanin-A influence the elevated hepatic enzyme level, such as AST, ALP, ALT, bilirubin, etc., and found to be a promising molecule in hepatotoxicity models
*AST↓,
*ALP↓,
*Bacteria↓, The results indicate that biochanin-A may be an effective alternate to antibiotics for alleviating SARA in cattles
*neuroP↑, the neuroprotective effects of biochanin-A might be attributed to the activation of the Nrf2 pathway and suppression of the NF-κB pathway
*SOD↑, Biochanin-A reduced oxidative stress in the brain by augmenting SOD (superoxide dismutase) and GSH-Px (glutathione peroxidase) and repressing MDA (malondialdehyde) levels.
*GPx↑,
*AChE↓, Acetylcholinesterase activity was found decreased in a dose-reliant manner amongst biochanin-A treated animals
*BACE↓, Biochanin-A non-competitively inhibited BACE1 with an IC 50 value of 28 μM.
*memory↑, estore learning and memory deficits in ovariectomized (OVX) rats.
*BioAv↓, The bioavailability of biochanin-A is poor.
TumCCA↑, BA exerted a significant cytotoxic effect on U937 cells through blocking cell cycle arrest at the G2/M phase and inducing apoptosis, and that the intracellular reactive oxygen species (ROS) levels increased after treatment with BA.
Apoptosis↑,
i-ROS↑,
cycA1/CCNA1↓, down-regulation of cyclin A and cyclin B1, and up-regulation of cyclin-dependent kinase inhibitor p21WAF1/CIP1 revealed the G2/M phase arrest mechanism of BA.
CycB/CCNB1↓,
P21↑,
Cyt‑c↑, BA induced the cytosolic release of cytochrome c by reducing the mitochondrial membrane potential with an increasing Bax/Bcl-2 expression ratio.
MMP↓,
Bax:Bcl2↑,
Casp9↑, BA also increased the activity of caspase-9 and -3, and subsequent degradation of the poly (ADP-ribose) polymerase.
Casp3↑,
PARP↓,
eff↓, However, quenching of ROS by N-acetyl-cysteine, an ROS scavenger, markedly abolished BA-induced G2/M arrest and apoptosis, indicating that the generation of ROS plays a key role in inhibiting the proliferation of U937 cells by BA treatment.
*antiOx↑, Accumulated evidence demonstrates that BA possesses various biological activities, including antioxidant, anti-inflammatory, hepatoprotective, and anti-tumor effects
*Inflam↓,
*hepatoP↑,
selectivity↑, BA are complex and depends on the type of cancer cells, without causing toxicity toward normal cells
NF-kB↓, Shen et al. (2019) recently reported that the suppression of the nuclear factor-kappa B pathway increased downstream oxidant effectors, thereby promoting the generation of reactive oxygen species (ROS) in BA-stimulated multiple myeloma cells.
*ROS↓, Although BA is known to have antioxidant activity that blocks the accumulation of ROS due to oxidative stress in normal cells (Cheng et al. 2019;
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AntiTum↑, BA is considered a future promising antitumor compound
Cyt‑c↑, BA stimulated mitochondria to release cytochrome c and Smac and cause further apoptosis reactions
Smad1↑,
Sepsis↓, Administration of 10 and 30 mg/kg of BA significantly improved survival against sepsis and attenuated lung injury.
NF-kB↓, BA inhibited nuclear factor-kappa B (NF-κB) expression in the lung and decreased levels of cytokine, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9)
ICAM-1↓,
MCP1↓,
MMP9↓,
COX2↓, In hPBMCs, BA suppressed cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PEG2) production by inhibiting extracellular regulated kinase (ERK) and Akt phosphorylation and thereby modulated the NF-κB signaling pathway
PGE2↓,
ERK↓,
p‑Akt↓,
*ROS↓, BA significantly decreased the mortality of mice against endotoxin shock and inhibited the production of PEG2 in two of the most susceptible organs, lungs and livers [80]. Moreover, BA reduced reactive oxygen species (ROS) formation
*LDH↓, and the release of lactate dehydrogenase
*hepatoP↑, hepatoprotective effect of BA from Tecomella undulata.
*SOD↑, Pretreatment of BA prevented the depletion of hepatic antioxidants superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) and ascorbic acid (AA) and decreased the CCl4-induced LPO level
*Catalase↑,
*GSH↑,
*AST↓, A also attenuated the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) plasma level,
*ALAT↓,
*RenoP↑, BA also exhibits renal-protective effects. Renal fibrosis is an end-stage renal disease symptom that develops from chronic kidney disease (CKD).
*ROS↓, BA protected against this ischemia-reperfusion injury in a mice model by enhancing blood flow and reducing oxidative stress and nitrosative stress
*α-SMA↓, Moreover, BA reduced the expression of α-smooth muscle actin (α-SMA) and collagen-I
*memory↑, Bacopa monnieri has been used for centuries in Ayurvedic medicine, alone or in combination with other herbs, as a memory and learning enhancer, sedative, and anti-epileptic.
*neuroP↑, Brahmi as a lead formulation for treating neurological disorders and exerting cognitive-enhancing effects.
*cognitive↑,
*hepatoP↑, figure 1
*antiOx↑,
*AntiDiabetic↑,
*fatigue↓,
*GSK‐3β↓, figure 3
*PI3K↑,
*Akt↑,
*tau↓,
*ROS↓, The neuroprotective properties of these bioactive components include reduction of ROS, neuroinflammation, aggregation inhibition of amyloid-β and improvement of cognitive and learning behavior.
*Inflam↓,
*hepatoP↑, However, it was found that Se protects the liver slightly better against CP damage than B
*ALAT↓, statistically significant difference was observed in the serum levels of ALT, AST, ALP, TAS, TOS and OSI.
*AST↓,
*ALP↓,
*NF-kB↓, A statistically significant difference was observed in serum levels of NF-kB, TNF-α, IL -1β, IL -6 and IL -10 when the Se + CP and B + CP-treated groups were compared with the CP-treated group
*TNF-α↓, fig 9
*IL1β↓,
*IL6↓,
*IL10↑,
*SOD↑, A statistically remarkable change in serum levels of SOD, CAT, GPx, MDA and GSH was observed in the group receiving only CP compared to groups Se, B and the control.
*Catalase↑,
*MDA↓, Fig 10
*GSH↑,
*GPx↑,
*antiOx↑, suggests that B and Se increase intracellular antioxidant status.
*NRF2↑, Se and B treatment can protect rat liver tissue from CP-induced oxidative stress, inflammation, and apoptosis by regulating Bax/Bcl-2 and Nrf2-Keap-1 signaling pathways.
*Keap1↓,
*Inflam↓, anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects.
*antiOx↑,
*ROS↓, The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing
*angioG↑, Boron compounds exhibit diverse therapeutic actions in wound healing, including antimicrobial effects, inflammation modulation, oxidative stress reduction, angiogenesis induction, and anti-fibrotic properties.
*COL1↑, Boron has been shown to increase the expression of proteins involved in wound contraction and matrix remodeling, such as collagen, alpha-smooth muscle actin, and transforming growth factor-beta1.
*α-SMA↑,
*TGF-β↑,
*BMD↑, Animals treated with boron showed favorable changes in bone density, wound healing, embryonic development, and liver metabolism
*hepatoP↑,
*TNF-α↑, BA elevates TNF-α and heat-shock proteins 70 that are related to wound healing.
*HSP70/HSPA5↑,
*SOD↑, antioxidant properties of BA showed that boron protects renal tissue from I/R injury via increasing SOD, CAT, and GSH and decreasing MDA and total oxidant status (TOS)
*Catalase↑,
*GSH↑,
*MDA↓,
*TOS↓,
*IL6↓, Boron supports gastric tissue by alleviating ROS, MDA, IL-6, TNF-α, and JAK2/STAT3 action, as well as improving AMPK activity
*JAK2↓,
*STAT3↓,
*AMPK↑,
*lipid-P↓, boron may improve wound healing by hindering lipid peroxidation and increasing the level of VEGF
*VEGF↑,
*Half-Life↝, Boron is a trace element, usually found at a concentration of 0–0.2 mg/dL in plasma with a half-life of 5–10 h, and 1–2 mg of it is needed in the daily diet
*hepatoP↑, to positively affect the liver metabolism, and to promote bone density, embryogenic development and wound healing, and is known to provide significant benefits in cancer treatment through neutron capture systems
*BMD↑,
*COX2↓, Increased skin inflammatory parameters (COX-2, IL-8, NF-KB, IL-6, and TNF-α) levels in UVB-exposed groups were inhibited in all treatment groups
*IL8↓,
*NF-kB↓,
*IL6↓,
*TNF-α↓,
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ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat-
ing the caspase-dependent pathway in human pancreatic
cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,
*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions
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*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,
*AST↓, Carvacrol supplementation (15 mg/kg body weight) significantly attenuated these alterations, thereby showing potent anticancer effect in liver cancer
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑,
*Catalase↑,
*GSH↑,
*GPx↑,
*GSR↑,
*hepatoP↑, These findings suggest that carvacrol prevents lipid peroxidation, hepatic cell damage, and protects the antioxidant system in DEN-induced hepatocellular carcinogenesis.
*lipid-P↓,
*lipid-P↓, Carvacrol also attenuated lipid peroxidation by reducing malondialdehyde (MDA) levels, while boosting total antioxidant capacity and improving inflammatory status.
*MDA↓,
*antiOx↑,
*Inflam↑,
RenoP↑, Moreover, restoration of liver and kidney function was observed through normalization of serum ALT, AST, urea, and creatinine levels
hepatoP↑,
*ALAT↓,
AST↓,
creat↓,
chemoPv↑, Preclinical studies have demonstrated the chemopreventive and therapeutic potential of Carvacrol in several malignancies, including breast cancer, melanoma, hepatocellular carcinoma, cervical cancer, and non-small cell lung cancer
Cyt‑c↑, markedly enhanced cytochrome c expression
FADD↑, . Carvacrol-injected therapy markedly elevated FADD expression
P53↑, Carvacrol receiving rat’s up-regulated P53 concentrations markedly that reached their peak in the injected (## P ≤ 0.01 vs. tumor and **P ≤ 0.01 vs. normal) as well as oral and mixed groups
AntiCan↑, Carvacrol has demonstrated strong anticancer properties by modulating multiple molecular pathways governing apoptosis, inflammation, angiogenesis, and metastasis.
Apoptosis↑,
Inflam↓,
angioG↓,
TumMeta↓,
selectivity↑, revealed its ability to selectively target cancer cells while sparing healthy tissue
BioAv↑, nanotechnology have further enhanced its pharmacological profile by improving solubility, stability, and tumor-targeted delivery.
ChemoSen↑, synergistic effects when used in combination with conventional chemotherapeutics.
Dose↝, 84.38% of OEO’s contents are ‘carvacrol’.
TumCP↓, limit metastasis, induce apoptosis, suppress tumor cell proliferation, and improve the effectiveness of traditional chemotherapy medications
hepatoP↑, Carvacrol shows biological activities, such as antimicrobial, antitumor, antimutagenic, antigenotoxic, anti-inflammatory, anti-angiogenic, hepatoprotective, and antihepatotoxic properties.
Casp3↑, induced apoptosis by activating caspase-3 and caspase-9 while downregulating Bcl-2 mRNA levels
Casp9↑,
Bcl-2↓,
ROS↑, carvacrol causes oxidative stress by increasing the production of reactive oxygen species (ROS) and depleting GSH levels, which results in strong lethal effects on AGS gastric cancer
GSH↓,
BAX↑, upregulating pro-apoptotic markers such as Bax, caspase-3, caspase-7, caspase-8, caspase-9, cytochrome C, Fas, Fas-associated death domain (FADD), and p53
Casp7↑,
Casp8↑,
Cyt‑c↑,
Fas↑,
FADD↑,
P53↑,
Bcl-2↓, downregulating anti-apoptotic Bcl-2.
TumMeta↓, preventing metastasis by limiting the migration and invasion of cancer cells by upregulating epithelial markers like E-Cadherin and tissue inhibitors of metalloproteinases 2 and 3 (TIMP2 and TIMP3)
TumCMig↓,
TumCI↓,
E-cadherin↑,
TIMP2↑,
TIMP3↑,
N-cadherin↓, downregulating mesenchymal markers like N-Cadherin and ZEB2
ZEB2↓,
*lipid-P↓, protects the liver from diethylnitrosamine (DEN)-induced hepatocellular carcinogenesis by reducing lipid peroxidation, restoring key liver enzymes (AST, ALT, ALP, LDH, cGT)
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑, and enhancing antioxidant defenses (SOD, CAT, GPx, GR, GSH)
*Catalase↑,
*GPx↑,
*GSR↑,
selectivity↑, while selectively inducing apoptosis in cancer cells without harming normal liver tissue
cl‑PARP↑, inhibits HepG2 cancer cell growth by activating caspase-3, promoting PARP cleavage, downregulating Bcl-2, and modulating the MAPK signaling pathway by selectively reducing ERK1/2 phosphorylation while activating p38
ERK↓,
p38↑,
OS↑, rats (aged 6–8 weeks) demonstrated that carvacrol enhances sorafenib efficacy in HCC, improving survival rates, reducing tumor progression, and mitigating sorafenib-induced cardiac and hepatic toxicity.
AFP↓, carvacrol reduces serum alpha-fetoprotein (AFP) and alpha-L-fucosidase (AFU) levels by downregulating COX-2 and oxidative stress, inhibits angiogenesis via VEGF suppression,
COX2↓,
VEGF↓,
PCNA↓, prevents tumor proliferation by downregulating proliferating cell nuclear antigen (PCNA) and Ki-67 through TNF-α suppression.
Ki-67↓,
TNF-α↓,
BioAv↓, Despite carvacrol’s promising effects in vitro and in vivo, limitations such as bioavailability and solubility challenge its therapeutic application.
Showing Research Papers: 1 to 50 of 177
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 177
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Ferroptosis↑, 1, GPx4↓, 1, GSH↓, 3, HO-1↑, 1, Iron↑, 1, ROS↓, 1, ROS↑, 10, i-ROS↑, 1, Thiols↓, 1,
Mitochondria & Bioenergetics ⓘ
MEK↓, 1, MMP↓, 5,
Core Metabolism/Glycolysis ⓘ
12LOX↓, 1, ALAT↓, 2, cMyc↓, 1, Glycolysis↓, 1, lactateProd↓, 1, TCA↓, 1,
Cell Death ⓘ
Akt↓, 2, p‑Akt↓, 2, Apoptosis↓, 1, Apoptosis↑, 8, BAD↓, 1, BAX↑, 4, Bax:Bcl2↑, 1, Bcl-2↓, 5, Bcl-2↑, 1, BIM↑, 1, Casp↑, 2, Casp1↑, 1, Casp12↑, 1, Casp3↑, 5, Casp7↑, 1, Casp8↑, 2, Casp9↑, 4, Cyt‑c↑, 7, DR5↑, 2, FADD↑, 2, Fas↑, 3, Ferroptosis↑, 1, JNK↑, 1, MAPK↓, 1, MAPK↑, 2, Mcl-1↓, 1, necrosis↑, 1, p38↑, 4, TumCD↑, 1,
Kinase & Signal Transduction ⓘ
RET↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
other↝, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, eIF2α↓, 1, ER Stress↑, 1, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
BNIP3↑, 1,
DNA Damage & Repair ⓘ
CHK1↓, 1, DNAdam↑, 2, P53↑, 3, PARP↓, 1, cl‑PARP↑, 3, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK4↓, 2, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 2, cycD1/CCND1↓, 3, cycE/CCNE↑, 1, P21↑, 4, TumCCA↑, 7,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 2, cMET↓, 1, CSCs↓, 2, EMT↓, 3, ERK↓, 5, GSK‐3β↓, 1, mTOR↓, 2, Nanog↓, 1, NOTCH↓, 1, NOTCH1↓, 1, PI3K↓, 5, SOX2↓, 1, STAT3↓, 3, TumCG↓, 3, Wnt↓, 2,
Migration ⓘ
AP-1↓, 1, Ca+2↑, 2, E-cadherin↓, 1, E-cadherin↑, 1, p‑FAK↓, 1, Ki-67↓, 2, MMP1↓, 1, MMP2↓, 4, MMP9↓, 6, MMPs↓, 1, N-cadherin↓, 1, PDGF↓, 1, Smad1↑, 1, SMAD4↓, 1, TGF-β↓, 1, TIMP2↑, 1, TIMP3↑, 1, TumCI↓, 3, TumCMig↓, 3, TumCP↓, 3, TumMeta↓, 5, uPA↓, 2, ZEB2↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 4, EGFR↓, 1, HIF-1↓, 1, Hif1a↓, 3, VEGF↓, 6, VEGFR2↓, 2,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CXCR4↓, 1, ICAM-1↓, 2, IL1β↓, 1, IL6↓, 3, IL8↓, 1, Inflam↓, 4, MCP1↓, 2, NF-kB↓, 6, PGE2↓, 1, TNF-α↓, 2,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, BioAv↝, 3, ChemoSen↑, 7, Dose↝, 1, eff↓, 1, eff↑, 2, MRP1↓, 1, RadioS↑, 1, selectivity↑, 4,
Clinical Biomarkers ⓘ
AFP↓, 1, ALAT↓, 2, ALP↓, 1, AR↓, 1, AST↓, 2, creat↓, 1, E6↓, 1, E7↓, 1, EGFR↓, 1, IL6↓, 3, Ki-67↓, 2,
Functional Outcomes ⓘ
AntiCan↓, 1, AntiCan↑, 6, AntiTum↑, 1, cardioP↑, 2, chemoP↑, 4, chemoPv↑, 1, cognitive↑, 1, hepatoP↑, 9, OS↑, 1, radioP↑, 1, RenoP↑, 1, toxicity↝, 1, TumVol↓, 1,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 160
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 23, Catalase↓, 1, Catalase↑, 13, Ferroptosis↓, 1, GPx↑, 9, GSH↓, 1, GSH↑, 16, GSR↑, 3, GSTA1↑, 1, GSTs↑, 2, HO-1↑, 2, Keap1↓, 2, lipid-P↓, 9, MDA↓, 15, MPO↓, 3, NRF2↑, 10, ROS?, 1, ROS↓, 22, SOD↓, 1, SOD↑, 18, TAC↑, 1, TBARS↓, 1, TOS↓, 1, uricA↓, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 15, AMPK↑, 3, p‑AMPK↑, 1, BUN↓, 1, GlucoseCon↑, 1, H2S↑, 1, LDH↓, 7, LDH↑, 1, PDH↑, 1, PDKs↓, 1, PKM2↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↓, 3, BAX↓, 1, cl‑Casp3↓, 1, Fas↓, 1, Ferroptosis↓, 1, iNOS↓, 2, JNK↓, 1, MAPK↓, 1, necrosis↓, 1,
Transcription & Epigenetics ⓘ
Ach↑, 1, other↑, 2,
Protein Folding & ER Stress ⓘ
CHOP↓, 1, ER Stress↓, 2, HSP70/HSPA5↑, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, LC3II↑, 1,
DNA Damage & Repair ⓘ
DNArepair↑, 1, cl‑PARP1↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 1, mTOR↑, 1, PI3K↓, 1, PI3K↑, 1, STAT3↓, 2, p‑STAT3↓, 1, TRPM7↓, 1,
Migration ⓘ
5LO↓, 1, AntiAg↑, 3, Ca+2↓, 1, COL1↑, 1, COL3A1↓, 1, MMP2↓, 1, MMP9↓, 1, TGF-β↑, 1, VCAM-1↓, 1, Vim↓, 1, α-SMA↓, 4, α-SMA↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, Hif1a↓, 1, Hif1a↑, 1, NO↓, 5, VEGF↓, 1, VEGF↑, 2,
Barriers & Transport ⓘ
BBB↑, 3, GLUT3↑, 1, GLUT4↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 7, CRP↓, 1, IKKα↓, 1, IL10↑, 3, IL1β↓, 3, IL6↓, 7, IL6↑, 1, IL8↓, 1, Imm↑, 3, Inflam↓, 18, Inflam↑, 1, JAK2↓, 1, p‑JAK2↓, 1, MCP1↓, 1, NF-kB↓, 9, PGE2↓, 3, TNF-α↓, 7, TNF-α↑, 2,
Synaptic & Neurotransmission ⓘ
5HT↑, 1, AChE↓, 1, BDNF↑, 2, ChAT↑, 1, tau↓, 1, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 1, BACE↓, 1, NLRP3↓, 2, β-Amyloid↓, 1,
Hormonal & Nuclear Receptors ⓘ
CYP19↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 1, BioAv↝, 2, BioEnh↑, 1, ChemoSen↑, 1, Dose↝, 5, eff↑, 6, Half-Life↝, 3,
Clinical Biomarkers ⓘ
ALAT↓, 15, ALP↓, 6, AST↓, 16, BG↓, 1, BMD↑, 2, BP↓, 1, creat↓, 2, CRP↓, 1, GutMicro↑, 3, IL6↓, 7, IL6↑, 1, LDH↓, 7, LDH↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, AntiDiabetic↑, 5, cardioP↑, 10, chemoPv↑, 1, cognitive↑, 6, fatigue↓, 1, hepatoP↑, 41, memory↑, 4, Mood↑, 1, motorD↑, 1, neuroP↑, 18, Obesity↓, 3, OS↑, 1, Pain↓, 2, RenoP↑, 9, toxicity↓, 3, toxicity↝, 2,
Infection & Microbiome ⓘ
Bacteria↓, 4,
Total Targets: 154
Scientific Paper Hit Count for: hepatoP, L,hepatoprotective
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
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