AMPK介导的二甲双胍抗心肌缺氧/复氧损伤的研究

Role of AMP-Activated Protein Kinase( AMPK) in Metformin Preconditioning Against Cardiomyocytes Anoxia/Reoxygenation Injury

目的研究二甲双胍对心肌细胞缺氧/复氧损伤的影响及腺苷酸激活的蛋白激酶(AMPK)在其中发挥的可能作用。方法将大鼠H9c2心肌样细胞随机分为正常对照组、缺氧/复氧组、二甲双胍组(加入终浓度为2 mmol/L的二甲双胍预处理12h);检测AMPK蛋白的表达情况,以及细胞存活率、培养液LDH活性、细胞SOD和GSH-Px活性。结果与正常对照组相比,经二甲双胍干预12 h后,H9c2心肌样细胞AMPK蛋白表达上调(P<0.01),细胞存活率上升,LDH活性下降,SOD及GSH-Px活性增加(P<0.01)。结论二甲双胍对缺氧/复氧H9c2心肌样细胞具有保护作用,其机制与激活AMPK有关。

OBJECTIVE To study the protective effect of metformin in anoxia / reoxygenation injury of H9c2 cardiomyocytes,and its molecular mechanism that may involving AMPK pathway. METHODS H9c2 cardiomyocytes of rats were randomly divided into 3groups： normal control group,A / R group and metformin pretreatment group（ cultured with 2 mmol / L metformin for 12 h）. The expression of AMPK,cell viability,LDH,SOD and GSH-Px activity were determined. RESULTS Compared with normal control,after 12 h metformin precondition,the expression of AMPK was up regulated in H9c2 cardiomyocytes（ P〈0. 01）. In the group pretreated with metformin before A / R,cell viability increased; the activity of LDH in culture medium decreased; the activity of intracellular SOD,GSH-Px increased（ P〈0.01）. CONCLUSION Metformin can protect H9c2 cardiomyocytes from A / R injury,and its molecular mechanism may involve AMPK pathway.