白藜芦醇对心肌肥大细胞内质网应激时GRP78和GRP94表达的影响

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目的:探讨白藜芦醇对异丙肾上腺素诱导的心肌细胞肥大的保护作用及对心肌肥大时内质网应激相关因子GRP78和GRP94表达的影响。方法:利用异丙肾上腺素诱导乳鼠心肌细胞建立心肌肥大细胞模型,将心肌细胞分为正常对照组、模型组(加入异丙肾上腺素0.3 mg/L作用48 h),白藜芦醇+异丙肾上腺素组(加入异丙肾上腺素0.3 mg/L和白藜芦醇11.4 mg/L作用48 h)和白藜芦醇对照组(加入白藜芦醇11.4 mg/L)。检测心肌细胞表面积和心肌肥大标志物ANP表达评价心肌细胞肥大程度,检测细胞培养液中乳酸脱氢酶(LDH)活性和丙二醛(MDA)含量;Western blot分析GRP78和GRP94的蛋白表达。结果:模型组与正常组比较,异丙肾上腺素作用心肌细胞48 h诱导心肌细胞肥大,内质网应激相关因子GRP78和GRP94蛋白表达均增高;白藜芦醇+异丙肾上腺素组与模型组比较,白藜芦醇(11.4 mg/L)干预可以有效抑制异丙肾上腺素诱导的细胞肥大,同时降低GRP78和GRP94的蛋白表达,减少细胞培养液中乳酸脱氢酶LDH和MDA的释放。结论:白藜芦醇通过抑制内质网应激相关因子GRP78和GRP94表达,减轻自由基生成发挥对心肌肥大的保护作用。 AIM: To investigate the protective effect of resveratrol on isoprenaline-induced cardiomyocyte hypertrophy and its effect on the expression of GRP78 and GRP94 in hypertrophic myocardium. Methods: Myocardial cells were induced by isoprenaline to establish a model of cardiac mast cells. Cardiomyocytes were divided into normal control group, model group (isoproterenol 0.3 mg / L for 48 h), resveratrol + Propranolol group (Isoproterenol 0.3 mg / L and Resveratrol 11.4 mg / L for 48 h) and resveratrol control group (Resveratrol 11.4 mg / L was added). The myocardial cell surface area and myocardial hypertrophy marker ANP expression were detected to evaluate the degree of cardiomyocyte hypertrophy, the activity of lactate dehydrogenase (LDH) and the content of malondialdehyde (MDA) in cell culture medium were detected. The protein expression of GRP78 and GRP94 was analyzed by Western blot. RESULTS: Compared with normal group, the isoprenaline-induced cardiomyocytes induced cardiomyocyte hypertrophy and the expressions of GRP78 and GRP94 protein in endoplasmic reticulum stress-related factors were increased. Compared with model group Compared with the control group, resveratrol (11.4 mg / L) could effectively inhibit isoprenaline-induced cell hypertrophy, decrease the protein expression of GRP78 and GRP94, and decrease the release of lactate dehydrogenase LDH and MDA in the cell culture medium. CONCLUSION: Resveratrol can inhibit the expression of GRP78 and GRP94, and reduce the protective effect of free radical on myocardial hypertrophy.
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