内质网应激信号通路在高脂诱导的心肌细胞损伤中的作用

发布时间：2018-10-25 08:33

【摘要】：目的探讨内质网应激信号通路在高脂诱导的心肌细胞损伤中的作用。方法棕榈酸(0.1~0.4 mmol·L~(-1))刺激心肌细胞(0~48 h),CCK-8法评估细胞生长状态,免疫印迹法评估细胞内内质网应激信号通路相关蛋白表达水平及细胞凋亡蛋白表达水平。结果棕榈酸(0.1~0.4 mmol·L~(-1))刺激H9C2心肌细胞24 h,0.2、0.4 mmol·L~(-1)组细胞增殖率均出现明显下降。棕榈酸(0.2 mmol·L~(-1))刺激H9C2心肌细胞时,24、48 h组细胞增殖率均出现明显下降。棕榈酸(0.2 mmol·L~(-1))刺激24 h,GRP78、CHOP、PERKphos、IRE1phos、ATF6等内质网应激相关蛋白及Bax蛋白表达均明显增高(P0.05),而Bcl-2表达出现明显降低(P0.05)。预处理内质网应激抑制剂普伐他汀(pravastatin,10mol·L~(-1))的棕榈酸(0.2 mmol·L~(-1))组与不加pravastatin的棕榈酸(0.2 mmol·L~(-1))组相比,Bcl-2及Bax的表达均恢复至正常水平。结论内质网应激信号通路对高脂引起的心肌损伤的发病及治疗均起到重要作用。
[Abstract]:Objective to investigate the role of endoplasmic reticulum stress signaling pathway in hyperlipidemic cardiomyocyte injury. Methods the growth status of cardiomyocytes was evaluated by palmitic acid (0.1 ~ 0.4 mmol L ~ (-1) (0 ~ 48 h), CCK-8), and the expression level of intracellular endoplasmic reticulum stress signal pathway associated protein and apoptotic protein were evaluated by Western blot. Results the proliferation rate of H9C2 cardiomyocytes stimulated by palmitic acid (0.1 ~ 0.4 mmol / L ~ (-1) at 24 h or 0.2 mmol L ~ (-1) was significantly decreased. When palmitic acid (0.2 mmol L ~ (-1) stimulated H9C2 cardiomyocytes, the proliferation rate of H9C2 cells decreased significantly in 24 h group. Palmitic acid (0.2 mmol L ~ (-1) increased the expression of ER stress-related protein and Bax protein (P0.05), while the expression of Bcl-2 decreased significantly (P0.05). The expression of Bcl-2 and Bax returned to normal level in pravastatin,10mol L ~ (-1) preconditioning group compared with pravastatin free palmitic acid (0.2 mmol L ~ (-1) group). Conclusion endoplasmic reticulum stress signaling pathway plays an important role in the pathogenesis and treatment of hyperlipidemic myocardial injury.
【作者单位】：武汉大学中南医院心血管内科;湖北科技学院糖尿病心脑血管病变湖北省重点实验室;
【基金】：湖北省教育厅科学研究计划资助项目(No B201696) 湖北科技学院糖尿病专项基金资助项目(No 2016-18XZ09);湖北科技学院博士启动基金资助项目(No BK1432)
【分类号】：R54;R587.2

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