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目的:研究晚期糖基化终产物(AGEs)对原代培养SD乳鼠心肌细胞的损伤,探讨内质网应激在AGEs诱导心肌细胞损伤中的作用。方法:原代培养SD大鼠乳鼠心肌细胞,随机分为对照组、AGEs组。MTT法检测心肌细胞存活率,Western blot法检测内质网应激蛋白GRP 78和CHOP蛋白表达水平。结果:与对照组相比,AGEs具有损伤心肌细胞的作用,并呈现剂量和时间依赖性;AGEs可以诱导内质网应激相关蛋白GRP 78和CHOP的高表达,并呈现剂量依赖性增加。结论:AGEs可以导致心肌细胞损伤,GRP 78和CHOP蛋白表达水平升高,提示内质网应激通路可能参与了AGEs诱导的心肌细胞损伤。
AIM: To investigate the effects of advanced glycation end products (AGEs) on cardiomyocytes in primary cultured neonatal SD rats and the role of endoplasmic reticulum stress in cardiomyocyte injury induced by AGEs. Methods: Primary cultured SD rat neonatal rat cardiomyocytes were randomly divided into control group and AGEs group. The survival rate of cardiomyocytes was detected by MTT assay and the expression of ER stress protein GRP 78 and CHOP protein were detected by Western blot. Results: Compared with the control group, AGEs could injure the cardiomyocytes in a dose-and time-dependent manner. AGEs could induce the overexpression of endoplasmic reticulum stress-related proteins GRP78 and CHOP in a dose-dependent manner. CONCLUSION: AGEs can induce cardiomyocyte injury and increase the expression of GRP 78 and CHOP protein, suggesting that endoplasmic reticulum stress pathway may be involved in AGEs-induced cardiomyocyte injury.