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目的:研究高交感活性诱导心肌氧化应激损伤受体依赖途径。方法:MTT法确定NE、H2O2诱导心肌细胞损伤模型,以心肌细胞存活率为60%确定NE、H2O2的浓度及作用时间;以普萘洛尔(Pro)、哌唑嗪(Praz)、维生素E(VE)为反向药物探针,以心肌细胞形态变化、MTT法、LDH活力及外漏率分析、SOD活力与MDA水平为检测指标,分析三者相互作用对NE诱导的心肌细胞损伤的保护作用。结果:NE在1μmol/L作用24h细胞存活率在60%,Pro、Praz、Pro+Praz(各1μmol/L)、Pro+Praz+VE(1+1+20μmol/L)及VE(20μmol/L)均能降低细胞损伤,提高SOD,降低MDA;而Pro+Praz对H2O2(200μmol/L)引起损伤未见明显保护作用,相反VE对H2O2及NE诱导的损伤均具有保护作用。结论:受体依赖是高交感活性诱导心肌氧化应激损伤的重要途径。
OBJECTIVE: To study the receptor-dependent pathway of high sympathetic activity-induced myocardial oxidative stress injury. Methods: MTT assay was used to determine the effects of NE and H2O2 on the injury of cardiomyocytes. The cardiomyocyte survival rate was 60%, and the concentration of NE and H2O2 and the action time were determined. The effects of propofol, Praz, (VE) as a reverse drug probe. The morphological changes of myocardial cells, MTT assay, LDH activity and leakage rate, SOD activity and MDA level were detected to detect the protective effect of the three interactions on NE-induced cardiomyocyte injury effect. RESULTS: The survival rate of NE was 60% after treated with 1μmol / L of NE for 1h, Pro + Praz, Pro + Praz (1μmol / L), Pro + Praz + VE (1 + 1 + 20μmol / L) and VE ) Could reduce cell injury, increase SOD and decrease MDA. However, Pro + Praz had no obvious protective effect on H2O2 induced injury. On the contrary, VE had a protective effect on H2O2 and NE-induced injury. CONCLUSION: Receptor dependence is an important pathway for the induction of myocardial oxidative stress induced by high sympathetic activity.