【摘要】 目的探讨氯沙坦对过氧化氢诱导心肌细胞凋亡的保护作用机制。方法在原代培养SD乳鼠心肌细胞上建立HO损伤模型,分别以低、中、高剂量(1、3、10μmol/L)氯沙坦、10μmol/L氯沙坦+50μmol/LLY294002处理,22检测各组心肌细胞存活率及丙二醛(MDA)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、caspase3/7、P-Akt蛋白表达。结果与HO组和LY294002组相比,不同剂量氯沙坦均可增加心肌细胞存活及LDH、SOD、P-Akt表达,减少MDA和22caspase3/7表达。结论氯沙坦对心肌细胞凋亡有抑制作用,可能与稳定细胞膜、抗脂质过氧化反应、清除氧自由基及激活PI3k/Akt信号通路有关。更多还原

【Abstract】 Ojective To investigate the protective mechanism of losartan on hydrogen peroxide-induced cardiocyte apoptos-is in suckling rats.Methods Primary cultured cardiocytes of suckling rats were used to establish H2O2-induced apoptosis model,and then treated with 1,3,and 10 μmol/L losartan,and 10 μmol/L losartan plus 50 μmol/L LY294002,respectively.Cardiocyte viability and levels of malonaldehyde(MDA),lactate dehydrogenase(LDH),superoxide dismutase(SOD),caspase3/7 and p-Akt were measured.Results Compared with H2O2 group and LY294002 group,cardiocyte viability and expression of LDH,SOD and P-Akt were upregulated,while that of MDA and caspase3/7 was downregulated in losartan group.Conclusion Losartan can inhibit H2O2-induced cardiocyte apoptosis in suckling rats via stabilizing cytomembrane,resisting lipid peroxidation,clearing oxygen free radical and activating PI3K/Akt pathway.更多还原