血管紧张素Ⅱ预处理对乳鼠心肌细胞缺氧复氧损伤的影响

Effect of angiotensin Preconditioning on anoxia reoxygenation injury of neonatal cardiac myocytes

观察血管紧张素Ⅱ预处理（ＡｎｇⅡ）对乳鼠心肌细胞缺氧复氧（Ａ／Ｒ）损伤的影响，并探讨其作用机理。采用心肌细胞Ａ／Ｒ损伤模型，用血管紧张素Ⅱ进行预处理（ＡⅡＰＣ）。ＡⅡＰＣ能提高Ａ／Ｒ损伤后心肌细胞存活率（７６±３％比５２±２％，Ｐ＜０．０１，减少细胞ＭＤＡ产生（０．９５±０．０６比１．７２±０．０７ｎｍｏｌ／ｍｇｐｒ，Ｐ＜０．０１），减少乳酸脱氢酶漏出（３６．５±７．１比５６．３±９．３Ｕ／Ｌ，Ｐ＜０．０１），及蛋白漏出（０．３３±０．０４比０．４３±０．０７ｇ／Ｌ，Ｐ＜０．０１）。蛋白激酶Ｃ（ＰＫＣ）抑制剂Ｈ７完全阻断ＡⅡＰＣ的上述保护作用。结果提示ＡⅡＰＣ对乳鼠心肌细胞具有预处理保护作用，其机理是通过ＰＫＣ介导的。

To investigate the effect of angiotensin preconditioning (A PC) on anoxia/reoxygenation (A/R) injury of neonatal rat cardiomyocytes and its mechanismOn the model of cardiomyocytes A/R,preconditioning was performed by angiotensin All PC can improve viability of cardiomyocytes during A/R injury (763% vs 522%,P<001),reduced formation of MDA (095006 vs 172007 nmol/mg pr,P<001),and leakage of LDH (36571 vs 56393 U/L,P<001),as well as leakage of protein (033004 vs 043007 g/L,P<001)Protein kinase C (PKC) inhibitorH7 can abolish all the protective effects of A PCThe results show that there is a protective effect of A PC on A/R injury of neonatal rat cardiomyocytes,and its mechanism is associated with activation of PKC