hepatoP Cancer Research Results
hepatoP, L,hepatoprotective: Click to Expand ⟱
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| Type: |
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⟱
toxicity↝, generally well tolerated. Eleven adverse events of grade 1 or grade 2 severity were observed. No grade 3 or grade 4 adverse events were observed.
hepatoP↓, Elevation of liver enzymes (5/11) and skin rash (2/11) was the most common adverse events.
BioAv↓, However, WA appears to have low oral bioavailability.
Apoptosis↑, WA has been reported to induce apoptosis via intrinsic and extrinsic pathways in human prostate, breast and leukemic cancer cells among others
ROS↑, It has also shown the ability to induce apoptosis in osteosarcoma U2OS cell lines by generating ROS, also causing cell cycle arrest in osteosarcoma cell lines by inhibition of G2/M checkpoint proteins
TumCCA↑,
TumCP↓, mechanism of action of celastrol in terms of inhibition of cell proliferation and regulation of the cell cycle, regulation of apoptosis and autophagy, inhibition of cell invasion and metastasis, anti-inflammation, regulation of immunotherapy, and an
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumCI↓,
TumMeta↓,
Imm↝,
angioG↓,
Cyt‑c↑, release of cytochrome c (CytC)
ROS↑, increasing ROS levels, and activating the mitochondrial apoptosis pathway
BAX↑, upregulating the expression of CytC and the pro-apoptotic protein Bax, activating caspase-3 and caspase-9, and leading to the cleavage of PARP
Casp3↑,
Casp9↑,
cl‑PARP↑,
PrxII↓, binds to peroxiredoxin-2 (Prdx2) and inhibits its enzyme activity,
ER Stress↑, resulting in ROS-dependent endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and apoptosis in gastric cancer cells
mtDam↑,
CHOP↑, celastrol upregulates the expression of CHOP, Bip, XBP1s, and IRE1 proteins,
Inflam↓, Anti-inflammatory properties of celastrol
NF-kB↓, Celastrol additionally obstructed NF-κB and its downstream gene products, such as CXCR4 and MMP9, and reduced serum IL-6 and TNF-α levels to inhibit cell invasion and migration in vivo
CXCR4↓,
MMP9↓,
IL6↓,
TNF-α↓,
HSP90↓, accumulation may be due to the inhibition of HSP90 and the stress response
neuroP↑, Our mass spectrometry research also showed that celastrol directly binds to HSP90 and HSP70, exerting antitumor and neuroprotective effects
STAT3↓, Celastrol exerts anti-tumor activity by inhibiting STAT3
Prx↓, celastrol binds directly to Prdx1, Prdx2, Prdx4, and Prdx6 via active cysteine sites, inhibiting their antioxidant activity without affecting protein expression
HO-1↑, Celastrol also targeted heme oxygenase-1 (HO-1), increasing its expression in activated hematopoietic stem cells
eff↑, Research has indicated that celastrol, combined with 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG), inhibits the toxic stress response of HSP90-targeted proteins, reduces the sensitization of human glioblastomas to celastrol treatment, an
eff↑, celastrol, when combined with EGFR tyrosine kinase inhibitors (EGFR-TKIs), effectively inhibits the growth and invasion of T790M mutant human lung cancer H1975
BioAv↑, nano-delivery systems present a novel pathway for the development and clinical application of celastrol, potentially overcoming existing limitations and maximizing its therapeutic potential.
toxicity↑, several significant challenges, including its pronounced hepatic and renal toxicity and potential for causing immunosuppression
CardioT↑, celastrol, which includes hepatotoxicity, cardiotoxicity, infertility toxicity, hematopoietic system toxicity and nephrotoxicity.
hepatoP↓,
*AntiCan↑, EGCG’s therapeutic potential in preventing and managing a range of chronic conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and metabolic syndromes
*cardioP↑,
*neuroP↑,
*BioAv↝, Factors such as fasting, storage conditions, albumin levels, vitamin C, fish oil, and piperine have been shown to affect plasma concentrations and the overall bioavailability of EGCG
*BioAv↓, Conversely, bioavailability is reduced by processes such as air oxidation, sulfation, glucuronidation, gastrointestinal degradation, and interactions with Ca2+, Mg2+, and trace metals,
*BioAv↓, EGCG’s oral bioavailability is generally low, with marked differences observed across species, for example, bioavailability rates of 26.5% in CF-1 mice and just 1.6% in Sprague Dawley rats
*Dose↝, plasma concentrations exceeded 1 μM only when doses of 1 g or higher were administered.
*Half-Life↝, Specifically, a dose of 1600 mg yielded a Cmax of 3392 ng/mL (range: 130–3392 ng/mL), with peak levels observed between 1.3 and 2.2 h, AUC (0–∞) values ranging from 442 to 10,368 ng·h/mL, and a half-life (t1/2z) of 1.9 to 4.6 h.
*BioAv↑, Studies on the distribution of EGCG have revealed that, despite its limited absorption, it is rapidly disseminated throughout the body or quickly converted into metabolites
*BBB↑, Additionally, EGCG can cross the blood–brain barrier, allowing it to reach the brain
*hepatoP↓, Several studies have documented liver damage linked to green tea consumption [48,49,50,51,52,53].
*other↓, EGCG has also been shown to inhibit the intestinal absorption of non-heme iron in a dose-dependent manner in a controlled clinical trial
*Inflam↓, EGCG has been widely recognized for its anti-inflammatory effects
*NF-kB↓, EGCG has been shown to suppress NF-κB activation, inhibit its nuclear translocation, and block AP-1 activity
*AP-1↓,
*iNOS↓, downregulation of pro-inflammatory enzymes like iNOS and COX-2 and scavenging of ROS/RNS, including nitric oxide and peroxynitrite
*COX2↓,
*ROS↓,
*RNS↓,
*IL8↓, EGCG has been shown to suppress airway inflammation by reducing IL-8 release, a cytokine involved in neutrophil aggregation and ROS production.
*JAK↓, EGCG blocks the JAK1/2 signaling pathway
*PDGFR-BB↓, downregulate PDGFR and IGF-1R gene expression
*IGF-1R↓,
*MMP2↓, reduce MMP-2 mRNA expression
*P53↓, downregulation of the p53-p21 signaling pathway and the enhanced expression of Nrf2
*NRF2↑,
*TNF-α↓, 25 to 100 μM reduced the levels of TNF-α, IL-6, and ROS while enhancing the expression of E2F2 and superoxide dismutases (SOD1 and SOD2), enzymes vital for cellular antioxidant defense.
*IL6↓,
*E2Fs↑,
*SOD1↑,
*SOD2↑,
Casp3↑, EGCG has been shown to activate key apoptotic pathways, such as caspase-3 activation, cytochrome c release, and PARP cleavage, in various cell models, including PC12 cells exposed to oxidative stress
Cyt‑c↑,
PARP↑,
DNMTs↓, (1) the inhibition of DNA hypermethylation by blocking DNA methyltransferase (DNMT)
Telomerase↓, (2) the repression of telomerase activity;
Hif1a↓, (3) the suppression of angiogenesis via the inhibition of HIF-1α and NF-κB;
MMPs↓, (4) the prevention of cellular metastasis by inhibiting matrix metalloproteinases (MMPs);
BAX↑, (5) the promotion of apoptosis through the activation of pro-apoptotic proteins like BAX and BAK
Bak↑,
Bcl-2↓, while downregulating anti-apoptotic proteins like BCL-2 and BCL-XL;
Bcl-xL↓,
P53↑, (6) the upregulation of tumor suppressor genes such as p53 and PTEN;
PTEN↑,
TumCP↓, (7) the inhibition of inflammation and proliferation via NF-κB suppression;
MAPK↓, (8) anti-proliferative activity through the modulation of MAPK and IGF1R pathways
HGF/c-Met↓, EGCG inhibits hepatocyte growth factor (HGF), which is involved in tumor migration and invasion
TIMP1↑, EGCG has also been shown to influence the expression of tissue inhibitors of metalloproteinases (TIMPs) and MMPs, which are involved in tumorigenesis
HDAC↓, nhibition of UVB-induced DNA hypomethylation and modulation of DNMT and histone deacetylase (HDAC) activities
MMP9↓, inhibiting MMPs such as MMP-2 and MMP-9
uPA↓, EGCG may block urokinase-like plasminogen activator (uPA), a protease involved in cancer progression
GlutMet↓, EGCG can exert antitumor effects by inhibiting glycolytic enzymes, reducing glucose metabolism, and further suppressing cancer-cell growth
ChemoSen↑, EGCG’s combination with standard chemotherapy drugs may enhance their efficacy through additive or synergistic effects, while also mitigating chemotherapy-related side effects
chemoP↑,
Glycolysis↓, fenbendazole and its promising anticancer biological activities, such as inhibiting glycolysis, down-regulating glucose uptake, inducing oxidative stress, and enhancing apoptosis in published experimental studies.
GlucoseCon↓,
ROS↑,
Apoptosis↑,
BioAv↓, Due to its poor absorption by oral administration, fenbendazole is particularly effective for targeting intestinal parasites
eff↑, Tippens began self-administering 222 mg fenbendazole orally, along with vitamin E supplements, CBD oil, and bioavailable curcumin. After three months of self-administration, a PET scan revealed no detectable cancer cells in his body.
toxicity↓, In rodents, its lethal dose (LD50) exceeded 10 g/kg, which is 1,000 times the therapeutic level
BioAv↑, vehicles for increasing the bioavailability of oral fenbendazole, it would be worthwhile to focus on dimethyl sulfoxide (DMSO), Salicylic acid, and methyl-β-cyclodextrin.
BioAv↑, Another method to improve the solubility of fenbendazole would be to complex it with methyl-β-cyclodextrin at a 1:1 ratio.
hepatoP↓, In both cases, despite the hepatotoxicity, patients’ liver function recovered rapidly upon discontinuing fenbendazole.
eff↑, combining fenbendazole with glycolysis inhibitors and hepatoprotective pharmaceutical or nutraceutical agents can lead to synergic therapeutic activity while reducing potential liver toxicity.
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
HO-1↑, 1, Prx↓, 1, PrxII↓, 1, ROS↑, 3,
Mitochondria & Bioenergetics ⓘ
mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
GlucoseCon↓, 1, GlutMet↓, 1, Glycolysis↓, 1,
Cell Death ⓘ
Apoptosis↑, 3, Bak↑, 1, BAX↑, 2, Bcl-2↓, 1, Bcl-xL↓, 1, Casp3↑, 2, Casp9↑, 1, Cyt‑c↑, 2, HGF/c-Met↓, 1, MAPK↓, 1, Telomerase↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNMTs↓, 1, P53↑, 1, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
HDAC↓, 1, PTEN↑, 1, STAT3↓, 1,
Migration ⓘ
MMP9↓, 2, MMPs↓, 1, TIMP1↑, 1, TumCI↓, 1, TumCP↓, 2, TumMeta↓, 1, uPA↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 1,
Immune & Inflammatory Signaling ⓘ
CXCR4↓, 1, IL6↓, 1, Imm↝, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 3, ChemoSen↑, 1, eff↑, 4,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
CardioT↑, 1, chemoP↑, 1, hepatoP↓, 3, neuroP↑, 1, toxicity↓, 1, toxicity↑, 1, toxicity↝, 1,
Total Targets: 58
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
NRF2↑, 1, RNS↓, 1, ROS↓, 1, SOD1↑, 1, SOD2↑, 1,
Cell Death ⓘ
iNOS↓, 1,
Transcription & Epigenetics ⓘ
other↓, 1,
DNA Damage & Repair ⓘ
P53↓, 1,
Cell Cycle & Senescence ⓘ
E2Fs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
IGF-1R↓, 1,
Migration ⓘ
AP-1↓, 1, MMP2↓, 1,
Angiogenesis & Vasculature ⓘ
PDGFR-BB↓, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL6↓, 1, IL8↓, 1, Inflam↓, 1, JAK↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 1, BioAv↝, 1, Dose↝, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cardioP↑, 1, hepatoP↓, 1, neuroP↑, 1,
Total Targets: 31
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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