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首页> 外文期刊>Diabetes, metabolic syndrome and obesity: targets and therapy >Protective Effects Of Astragalus Polysaccharides On Oxidative Stress In High Glucose-Induced Or SOD2-Silenced H9C2 Cells Based On PCR Array Analysis
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Protective Effects Of Astragalus Polysaccharides On Oxidative Stress In High Glucose-Induced Or SOD2-Silenced H9C2 Cells Based On PCR Array Analysis

机译:黄芪多糖对高葡萄糖诱导或SOD2沉默H9C2细胞氧化应激的保护作用基于PCR阵列分析

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Background: Oxidative stress in cardiac myocytes is an important pathogenesis of diabetic cardiomyopathy (DCM). Previously, we reported that astragalus polysaccharide (APS) has protective effects against the oxidative stress of DCM. This study aimed to determine the effect of APS on the oxidative stress induced by hyperglycemia in H9C2 cells. Methods: Rat H9C2 cells were cultured in vitro and randomly divided into the control group, HG group, APS-HG group, siRNASOD2 group, and APS-siRNASOD2 group. The cellular ultrastructure was measured by transmission electron microscopy. Cell apoptosis was examined by TUNEL staining. Levels of reactive oxygen species (ROS) were detected by a quantitative fluorescence assay (DHE). 8-OH-dG and nitrotyrosine, the indicators of oxidative stress injury, were detected by immunohistochemistry. A PCR array was used to evaluate the expression levels of 84 oxidative stress genes in cultured cells, and the PCR array results were partially verified by Western blot. Results: APS treatment protected the H9C2 cell ultrastructure, reduced the level of cell apoptosis, inhibited cellular ROS production, and reduced the levels of oxidative stress injury indicators 8-OH-dG and nitrotyrosine in high glucose-induced or SOD2-silenced H9C2 cells. It also altered oxidative stress-related genes at the mRNA and protein levels. Conclusion: APS may improve antioxidant capacity and inhibit oxidative stress injury in high glucose induced H9C2 cells.
机译:背景:心肌细胞中的氧化应激是糖尿病心肌病(DCM)的重要发病机制。以前,我们报道了黄芪多糖(AP)对DCM的氧化应激具有保护作用。该研究旨在确定APS对H9C2细胞高血糖血症诱导的氧化应激的影响。方法:大鼠H9C2细胞在体外培养并随机分为对照组,Hg组,APS-Hg组,SiRNASOD2组和APS-SIRNASOD2组。通过透射电子显微镜测量细胞超微结构。 Tunel染色检查细胞凋亡。通过定量荧光测定(DHE)检测反应性氧物质(ROS)水平。 8-OH-DG和硝基吡啉,通过免疫组化检测氧化胁迫损伤的指标。使用PCR阵列来评估培养细胞中84个氧化应激基因的表达水平,并通过Western印迹部分验证PCR阵列结果。结果:APS治疗保护H9C2细胞超微结构,降低细胞凋亡水平,抑制细胞ROS生产,并降低了高葡萄糖诱导或SOD2-沉默的H9C2细胞中的氧化应激损伤指标8-OH-DG和硝基滴水的水平。它还改变了mRNA和蛋白质水平的氧化应激相关基因。结论:APS可以改善抗氧化能力并抑制高葡萄糖诱导的H9C2细胞中的氧化应激损伤。

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