【摘要】 目的研究内皮素-1-内皮素受体A通路在高血糖导致的心肌损伤中发挥的作用。方法利用大鼠乳鼠原代心肌细胞构建高糖损伤模型。利用实时RT-PCR和细胞免疫荧光染色分别检测BNP在基因和蛋白水平的表达量。通过TMRM染色评价线粒体膜电位和氧化应激反应。通过免疫荧光染色测量心肌细胞面积,反映心肌细胞损伤状态。结果高糖培养导致心肌细胞表面积增大,线粒体膜电位增加,BNP在基因水平和蛋白水平表达上调,同时导致ETA表达上调,且恢复低糖培养后心肌损伤和ETA上调均不能完全恢复,但ETA受体波生坦能够逆转高糖造成的心肌损伤。结论高糖能够造成心肌细胞损伤,并产生代谢记忆效应,ETA在高糖刺激后的持续高表达可能是造成代谢记忆效应的重要原因。更多还原

【Abstract】 Objective To evaluate the role of endothelin-l-endothelin A receptor in high glucose induced cardiomyocyte injury. Methods Neonatal rats ventricular cardiomyocytes(NRVMs) were subjected to medium with 25 mmol/L glucose for the induction of high glucose related cardiomyocyte injury. Natriuretic peptide B(BNP), mitochondrial membrane potential(MMP) and cell surface area were used to evaluate NRVMs injury. mRNA expression of endothelin A receptor(ETA) was detected with qPCR. Results High glucose could increase the expression of BNP in both mRNA and protein level. Cell surface area and MMP were also increased in high glucose environment. High glucose induced NRVMs injury couldn’t be reversed by hypoglycemic therapy. ETA was upregulated by stimulation of high glucose and couldn’t be decreased by hypoglycemic therapy. Conclusion High glucose induced upregulation of ETA plays an important role in high glucose induced cardiomyocytes injury. It may be a therapeutic target in the treatment of diabetes related cardiovascular complications.更多还原