摘要
目的:探讨普罗布考对过氧化氢(H2O2)诱导的心肌细胞凋亡的影响,探讨其可能的机制。方法:培养的新生大鼠心肌细胞随机分组,分别给予0、1、10和100μmol/L普罗布考预处理6h后,再给予0.2mmol/LH2O2继续孵育6h。采用流式细胞仪检测细胞凋亡率,RT-PCR法检测细胞Bcl-2及BaxmRNA的表达,黄嘌呤氧化酶法测定细胞内超氧化物歧化酶(SOD)活性,硫代巴比妥酸法检测细胞内丙二醛(MDA)含量。结果:普罗布考剂量依赖性地抑制H2O2诱导的心肌细胞凋亡,降低心肌细胞BaxmRNA表达,升高Bcl-2mRNA表达,升高心肌细胞SOD活性,降低MDA含量。结论:普罗布考可抑制H2O2诱导的乳鼠心肌细胞凋亡,其作用机制与改善心肌细胞氧化应激水平有关。
Aim：To observe the effect of probucol on cardiomyocyte apoptosis induced by hydrogen peroxide（H 2 O2） and to explore its possible mechanisms.Methods：Cultured neonatal rat cardiomyocytes were randomly divided into 4 groups,and were given 0,1,10,and 100μmol/L probucol pretreatment for 6 h,respectively,and then induced by 0.2 mmol/L H2 O2 for 6 h.Apoptosis cells were assessed by flow cytometry.The mRNA expression of Bcl-2 and Bax in cardiomyocytes was determined by RT-PCR.The superoxide dismutase（SOD）activity and malondialdehyde（MDA）contents in cells were tested by xanthine oxidase method and color reaction of thiobarbituric acid method,respectively.Results：Probucol decreased cardiomyocyte apoptosis induced by H2 O2 and Bax mRNA expression,increased Bcl-2 mRNA expression,increased SOD activity and decreased the MDA content significantly.All these effects were in a dose-dependent manner.Conclusion：Probucol could inhibit cardiomyocyte apoptosis induced by H 2 O2 partly by reducing the oxidative stress level.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2011年第6期846-849,共4页
Journal of Zhengzhou University(Medical Sciences)
基金
河南省科技厅基础与前沿项目资助课题112300410049
