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首页> 外文期刊>European review for medical and pharmacological sciences. >Polyphenol epigallocatechin-3-gallate alleviates high glucose-induced H9C2 cell damage through PI3K/Akt pathway
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Polyphenol epigallocatechin-3-gallate alleviates high glucose-induced H9C2 cell damage through PI3K/Akt pathway

机译:多酚表没食子儿茶素-3-没食子酸酯通过PI3K / Akt途径减轻高糖诱导的H9C2细胞损伤

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OBJECTIVE: The aim of this work was to study the protective effect of polyphenol epigallocatechin-3-gallate (EGCG) on high glucose-induced oxidative damage of H9C2 cells and to investigate the relationship between this effect and phosphatidyl inositol 3 kinase-serine/threonine kinase (P13K/Akt) signal transduction pathway. MATERIALS AND METHODS: H9C2 cells were used as objects of study, 350 mM glucose serum-free medium was used as the high glucose molding condition, and LY294002 (10 μM) was used as the PI3K/Akt inhibitor. 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide (MTT) assay was used to detect the cell viability, lactate dehydrogenase (LDH) assay was used to detect the cytotoxicity, flow cytometry was used to detect the proportion of cell apoptosis, and Western blotting was used to detect the expressions of cell-associated proteins. RESULTS: Cell viability was reduced and cell apoptosis was increased by 350 mM high glucose. The high glucose-induced apoptosis was alleviated and the Akt expression in cells was increased by EGCG. The protective effect of EGCG was reduced after inhibition of PI3K/Akt pathway. CONCLUSIONS: EGCG protects H9C2 cells from high glucose-induced damage. EGCG plays the protective effect through inducing the PI3K/Akt pathway activation.
机译:目的:研究多酚表没食子儿茶素-3-没食子酸酯(EGCG)对高糖诱导的H9C2细胞氧化损伤的保护作用,并探讨该作用与磷脂酰肌醇3激酶丝氨酸/苏氨酸的关系。激酶(P13K / Akt)信号转导途径。材料与方法:以H9C2细胞为研究对象,以350 mM无葡萄糖葡萄糖血清培养基为高葡萄糖成型条件,以LY294002(10μM)作为PI3K / Akt抑制剂。 3-(4,5-二甲基噻唑-2-基)2,5-二苯基溴化四唑(MTT)法检测细胞活力,乳酸脱氢酶(LDH)法检测细胞毒性,流式细胞仪检测检测细胞凋亡的比例,并使用蛋白质印迹法检测细胞相关蛋白的表达。结果:350 mM高糖可降低细胞活力,并增加细胞凋亡。 EGCG减轻了高葡萄糖诱导的细胞凋亡,并增加了细胞中Akt的表达。抑制PI3K / Akt途径后,EGCG的保护作用降低。结论:EGCG可保护H9C2细胞免受高糖诱导的损伤。 EGCG通过诱导PI3K / Akt途径激活发挥保护作用。

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