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首页> 外文期刊>BMC Complementary and Alternative Medicine >The effect of Astragalus polysaccharides on attenuation of diabetic cardiomyopathy through inhibiting the extrinsic and intrinsic apoptotic pathways in high glucose -stimulated H9C2 cells
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The effect of Astragalus polysaccharides on attenuation of diabetic cardiomyopathy through inhibiting the extrinsic and intrinsic apoptotic pathways in high glucose -stimulated H9C2 cells

机译:黄芪多糖通过抑制高糖刺激的H9C2细胞外源性和内在性凋亡途径减轻糖尿病性心肌病的作用

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Background Apoptosis plays a critical role in the progression of diabetic cardiomyopathy (DC). Astragalus polysaccharides (APS), an extract of astragalus membranaceus (AM), is an effective cardioprotectant. Currently, little is known about the detailed mechanisms underlying cardioprotective effects of APS. The aims of this study were to investigate the potential effects and mechanisms of APS on apoptosis employing a model of high glucose induction of apoptosis in H9C2 cells. Methods A model of high glucose induction of H9C2 cell apoptosis was adopted in this research. The cell viabilities were analyzed by MTT assay, and the apoptotic response was quantified by flow cytometry. The expression levels of the apoptosis related proteins were determined by Real-time PCR and western blotting. Results Incubation of H9C2 cells with various concentrations of glucose (i.e., 5.5, 12.5, 25, 33 and 44?mmol/L) for 24?h revealed that cell viability was reduced by high glucose dose-dependently. Pretreatment of cells with APS could inhibit high glucose-induced H9C2 cell apoptosis by decreasing the expressions of caspases and the release of cytochrome C from mitochondria to cytoplasm. Further experiments also showed that APS could modulate the ratio of Bcl-2 to Bax in mitochondria. Conclusions APS decreases high glucose-induced H9C2 cell apoptosis by inhibiting the expression of pro-apoptotic proteins of both the extrinsic and intrinsic pathways and modulating the ratio of Bcl-2 to Bax in mitochondria.
机译:背景凋亡在糖尿病性心肌病(DC)的进展中起着至关重要的作用。黄芪多糖(APS)是黄芪膜(AM)的提取物,是一种有效的心脏保护剂。目前,关于APS的心脏保护作用的详细机制知之甚少。这项研究的目的是使用高糖诱导H9C2细胞凋亡的模型研究APS对凋亡的潜在作用及其机制。方法采用高糖诱导H9C2细胞凋亡的模型。通过MTT测定法分析细胞活力,并通过流式细胞术定量凋亡反应。通过实时PCR和蛋白质印迹法测定凋亡相关蛋白的表达水平。结果将各种浓度的葡萄糖(分别为5.5、12.5、25、33和44?mmol / L)的H9C2细胞孵育24小时,发现高葡萄糖剂量依赖性地降低了细胞活力。用APS预处理细胞可以通过减少胱天蛋白酶的表达和从线粒体到细胞质的细胞色素C的释放来抑制高糖诱导的H9C2细胞凋亡。进一步的实验还表明,APS可以调节线粒体中Bcl-2与Bax的比例。结论APS通过抑制外在和内在途径的促凋亡蛋白的表达以及调节线粒体中Bcl-2与Bax的比率来减少高糖诱导的H9C2细胞凋亡。

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