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epigallocatechin/hypoxie
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Seite 1 von 68 Ergebnisse
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.
Hypoxia-stimulated vascular endothelial growth factor production in human nasal polyp fibroblasts: effect of epigallocatechin-3-gallate on hypoxia-inducible factor-1 alpha synthesis.
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OBJECTIVE
To verify the inhibitory effects of epigallocatechin-3-gallate (EGCG) on the synthesis of hypoxia-induced vascular endothelial growth factor (VEGF) in nasal polyp fibroblasts (NPFs).
METHODS
Eight primary cultures of NPFs were established from nasal polyps. Effects of EGCG on the
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
Epigallocatechin-3-Gallate Attenuates Adriamycin-Induced Focal Segmental Glomerulosclerosis via Suppression of Oxidant Stress and Apoptosis by Targeting Hypoxia-Inducible Factor-1α/ Angiopoietin-Like 4 Pathway.
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Polyphenol epigallocatechin-3-gallate inhibits hypoxia/reoxygenation-induced H9C2 cell apoptosis.
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BACKGROUND
We aimed to observe the protective effect of EGCG on hypoxia/reoxygenation injury of H9C2 myocardial cells and to study the inhibition mechanism of EGCG on hypoxia/reoxygenation injury of H9C2 myocardial cells.
METHODS
H9C2 cells were used as the objects of study and hypoxia/reoxygenation
Epigallocatechin-3-gallate ameliorates hypoxia-induced pulmonary vascular remodeling by promoting mitofusin-2-mediated mitochondrial fusion.
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Pulmonary hypertension (PH) mainly results from excessive proliferation of pulmonary artery smooth muscle cells (PASMCs) and displays mitochondrial abnormalities such as mitochondrial fragmentation. Epigallocatechin-3-gallate (EGCG), an efficient antiproliferative compound in green tea, has recently
Comparison of effects of epigallocatechin-3-gallate on hypoxia injury to human umbilical vein, RF/6A, and ECV304 cells induced by Na(2)S(2)O(4).
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Hypoxia is related to the etiology of numerous pathological disease states, such as the formation of tumors or diverse retinopathies. Epigallocatechin-3-gallate (EGCG), a potent polyphenolic antioxidant and antiangiogenic compound found in green tea, has been shown to suppress the growth of blood
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"
Green tea extract and (-)-epigallocatechin-3-gallate inhibit hypoxia- and serum-induced HIF-1alpha protein accumulation and VEGF expression in human cervical carcinoma and hepatoma cells.
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Green tea extract and its major component (-)-epigallocatechin-3-gallate (EGCG) exhibit antiangiogenic activities in various experimental tumor models. A growing body of evidence has established that hypoxia-inducible factor-1alpha (HIF-1alpha) and its downstream target, vascular endothelial growth
Epigallocatechin-3-gallate and zinc provide anti-apoptotic protection against hypoxia/reoxygenation injury in H9c2 rat cardiac myoblast cells.
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It has previously been demonstrated that phosphatidylinositol-3-kinase (PI3K)/Akt and cleaved caspase-3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. Epigallocatechin-3-gallate (EGCG), the predominant catechin component of green tea, has been
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
Regulation of Neprilysin Activity and Cognitive Functions in Rats After Prenatal Hypoxia.
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The amyloid-degrading enzyme neprilysin (NEP) is one of the therapeutic targets in prevention and treatment of Alzheimer's disease (AD). As we have shown previously NEP expression in rat parietal cortex (Cx) and hippocampus (Hip) decreases with age and is also significantly reduced after prenatal
[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
(-)-Epigallocatechin-3-gallate attenuates myocardial injury induced by ischemia/reperfusion in diabetic rats and in H9c2 cells under hyperglycemic conditions.
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(-)-Epigallocatechin gallate (EGCG) exerts multiple beneficial effects on cardiovascular performance. In this study, we aimed to examine the effects of EGCG on diabetic cardiomyopathy during myocardial ischemia/reperfusion (I/R) injury. EGCG (100 mg/kg/day) was administered at week 6 for 2 weeks to
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