中文摘要：

目的探讨吡格列酮对缺氧复氧诱导的乳鼠心肌细胞凋亡和心肌细胞ATP敏感性钾通道亚单位表达的影响。方法原代培养的sD乳鼠心肌细胞随机分为6组：溶媒组、缺氧复氧组、0．1μmol／L吡格列酮组、1．0μmol／L吡格列酮组、2．0μmol／L吡格列酮组、2．0μmol／L吡格列酮＋GW9662组（GW9662组），药物预处理24h后建立缺氧复氧模型，利用膜联蛋白-v与溴化丙啶双染法检测心肌细胞凋亡，利用RT—PCR及Western—blot技术检测心肌细胞ATP敏感性钾通道亚单位的表达。结果0．1、1．0、2．0μmol／L吡格列酮组心肌细胞凋亡率与缺氧复氧组及GW9662组比较差异有统计学意义（P〈0．05）；0．1、1．0、2．0μmol／L吡格列酮组心肌细胞线粒体ATP敏感性钾通道（mitoKATP）亚单位Kir6．1mRNA及蛋白的表达与缺氧复氧组及GW9662组比较差异有统计学意义（P〈0．05），各组细胞膜ATP敏感性钾通道（sarcKATP）亚单位Kir6．2mRNA表达间差异无统计学意义（P〉0．05）。结论吡格列酮抑制缺氧复氧诱导的乳鼠心肌细胞凋亡，此保护作用可能与激活PPARγ及上调mitoKATP通道亚单位表达有关，sarcKATP未参与这种保护过程。

英文摘要：

Objective To investigate the effect of pioglitazone on hypoxia -reoxygenation -induced apoptosis in neonatal rat cardiac myoeytes and on ATP - sensitive potassium channel subunit expression. Methods Primarily cultured SD neo- natal rat eardiomyocytes were randomly divided into groups A （ menstruum group ）, B （ hypoxia - reoxygenation group ）, C （treated with 0. 1μmol/L pioglitazone）, D （with 1 μLmoL/L）, E （with 2 μmol/L）, F （with 2 μmo]/L piogiitazone ＋ PPARγ, specific antagonist GW9662）. Hypoxia - reoxygenation models were established after 24 h of drug pre - treatment, and apoptoses of myocardial cells were detected by annexin - v and FITC/PI, and APT - sensitive potassium channel subunit expression by RT - PCR and Western - blot. Results Groups C, D, E were significantly different from groups B, F in myocardial apoptosis rate （ P 〈 0. 05 ）, and in myocardial mitochondrial ATP - sensitive potassium channel （mitoKATP） subunit Kir6. 1 mRNA and protein expressions （P 〈 0. 05 ）, but there was not difference in membrane ATP - sensitive potassium channel （sarcKATP） subunit Kir6. 2 mRNA expressions between all groups （ P 〉 0. 05 ）. Conclusion Pretreatment with pioglitazone can reduce hypoxia - reoxygcnation - induced myocardial cells apoptosis in neonatal rats, which may related with activated PPAR~/and up - regulated mitoKATP channel subunit expression, and in which sarcKATP dose not involved.