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epigallocatechin gallate/hypoxia
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The reduction of hypoxia-induced and reoxygenation-induced apoptosis in rat islets by epigallocatechin gallate.
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The survival of transplanted tissue is affected by the detrimental consequences of hypoxia followed by reoxygenation. The majority of transplanted cells undergo apoptosis due to hypoxia and reoxygenation (H/R) injury, but protection from H/R has been less examined. In this study, we examined whether
Epigallocatechin gallate reduces hypoxia-induced apoptosis in human hepatoma cells.
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Cell detachment from extracellular matrix is closely related to induction of apoptosis. Epigallocatechin gallate (EGCG) has been shown to have antioxidant effect and to protect hypoxia-induced damage. We investigated whether EGCG reduced hypoxia-induced apoptosis and cell detachment in HepG2 cells.
Neuroprotective effects of (-)-epigallocatechin gallate following hypoxia-ischemia-induced brain damage: novel mechanisms of action.
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(-)-Epigallocatechin gallate (EGCG) is a potent antioxidant that is neuroprotective against ischemia-induced brain damage. However, the neuroprotective effects and possible mechanisms of action of EGCG after hypoxia-ischemia (HI) have not been investigated. Therefore, we used a modified "Levine"
Effect of saliva, epigallocatechin gallate and hypoxia on Cu-induced oxidation and cytotoxicity.
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We have previously reported that contact with copper (Cu) induced immediate cell death via an oxidation-involved mechanism in human promyelocytic leukemic HL-60 cells, whereas contact with other metals (Au, Ag, Pd) produced no discernible effect. In the present study, we investigated the conditions
[Effect of antioxidants on human primary and metastatic colon cancer cells at hypoxia and normoxia].
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OBJECTIVE
Evaluation of some antioxidants on human colon cancer cells viability and proliferation at various oxygen levels.
METHODS
Human primary (SW480) and metastatic (SW620) colon cancer cells were cultured at hypoxia (1% oxygen), tissues (10% oxygen) and atmospheric (21% oxygen) normoxia with
Propofol inhibits hypoxia/reoxygenation-induced human gastric epithelial cell injury by suppressing the Toll-like receptor 4 pathway.
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This study aimed to investigate the role of the Toll-like receptor 4 (TLR4) pathway in normal human gastric epithelial (GES-1) cells under hypoxia/reoxygenation (H/R) in vitro, and the effect of propofol on injured GES-1 cells as well as its possible mechanism. Before H/R induction, GES-1 cells were
Inactivation of prolyl hydroxylase domain (PHD) protein by epigallocatechin (EGCG) stabilizes hypoxia-inducible factor (HIF-1α) and induces hepcidin (Hamp) in rat kidney.
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HIF-1α plays a key role in iron uptake and transport in the liver, whose activity is tightly linked to the repression of hepcidin (Hamp). Hamp prevents intestinal iron uptake and cellular efflux by negatively modulating ferroportin. Hamp is also expressed in the kidneys, where transcriptional
[Effect of epigallocatechin gallate against exercise-induced fatigue in mice].
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OBJECTIVE
To investigate the effects of epigallocatechin gallate (EGCG)against exercise-induced fatigue in mice.
METHODS
Total 120 mice were randomly divided into three groups and tested separately. For each test, there were 30 mice subdivided into high dose (50 mg/kg . d EGCG) and low dose (10
Green tea polyphenol (-)-epigallocatechin gallate attenuates the neuronal NADPH-d/nNOS expression in the nodose ganglion of acute hypoxic rats.
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Recent studies have shown that (-)-epigallocatechin gallate (EGCG), one of the green tea polyphenols, has a potent antioxidant property. Nitric oxide (NO) plays an important role in the neuropathogenesis induced by brain ischemia/reperfusion and hypoxia. This study aimed to explore the potential
Green tea polyphenol (-)-epigallocatechin gallate prevents oxidative damage on periventricular white matter of infantile rats with hydrocephalus.
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Hydrocephalus causes damage to periventricular white matter at least in part through chronic ischemia. Emphasizing the periventricular ischemia/hypoxia in hydrocephalus, various authors indicated the secondary biochemical impairment and oxidative damage in experimentally induced and congenital
(-)-Epigallocatechin Gallate Promotes MicroRNA 145 Expression against Myocardial Hypoxic Injury through Dab2/Wnt3a/β-catenin.
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MicroRNA 145 (miR-145) is a critical modulator of cardiovascular diseases. The downregulation of myocardial miR-145 is followed by an increase in disabled-2 (Dab2) expression in cardiomyocytes. (-)-epigallocatechin gallate (EGCG) is a flavonoid that has been evaluated extensively due to its diverse
Epigallocatechin gallate but not catechin prevents nonalcoholic steatohepatitis in mice similar to green tea extract while differentially affecting the gut microbiota
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Catechin-rich green tea extract (GTE) protects against nonalcoholic steatohepatitis (NASH) by alleviating gut-derived endotoxin translocation and hepatic Toll-like receptor-4 (TLR4)-nuclear factor κB (NFκB) inflammation. We hypothesized that intact GTE would attenuate NASH-associated responses along
EGCG protects cardiomyocytes against hypoxia-reperfusion injury through inhibition of OMA1 activation.
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Mitochondria are important for energy production and cardiomyocyte homeostasis. OMA1, a metalloendopeptidase, initiates the proteolytic process of the fusion-allowing protein OPA1, to deteriorate mitochondrial structure and function. In this study, mouse embryonic fibroblasts (MEFs) and neonatal
Epigallocatechin gallate inhibits HIF-1alpha degradation in prostate cancer cells.
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Hypoxia-inducible factor-1, an alphabeta heterodimeric transcription factor, consists of a constitutively expressed HIF-1beta subunit and a hypoxia-inducible HIF-1alpha subunit, and contributes to hypoxia-mediated tumor angiogenesis. Numerous epidemiologic and laboratory studies indicate that green
(-)-Epigallocatechin gallate inhibits growth and activation of the VEGF/VEGFR axis in human colorectal cancer cells.
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(-)-Epigallocatechin gallate (EGCG), the major constituent of green tea, inhibits the growth of colorectal cancer cells by inhibiting the activation of various types of receptor tyrosine kinases (RTKs). The RTK vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) axis induces tumor
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