| 丙酮酸乙酯对大鼠心肌缺血再灌注细胞凋亡及Bcl-2、Bax蛋白表达的影响 |
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| 引用本文： | 郭家龙,张凯伦,蒋雄刚,夏家红,孙宗全. 丙酮酸乙酯对大鼠心肌缺血再灌注细胞凋亡及Bcl-2、Bax蛋白表达的影响[J]. 华中科技大学学报(医学版), 2007, 36(2): 262-264 |
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| 作者姓名： | 郭家龙 张凯伦 蒋雄刚 夏家红 孙宗全 |
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| 作者单位： | 华中科技大学同济医学院附属协和医院心血管外科,武汉,430022 |
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| 摘 要： | 目的研究丙酮酸乙酯（EP）对缺血／再灌注（I／R）心肌细胞凋亡及Bcl-2、Bax蛋白表达的影响，探讨其抑制缺血／再灌注心肌细胞凋亡的可能机制。方法应用Langendorff主动脉逆行灌流的体外大鼠缺血／再灌注心脏模型，24只雄性大鼠随机分为3组（每组各8只）：对照组，K—H液持续灌流120min；缺血／再灌注组，平衡灌流30min，全心停灌30min，再灌60min；EP组，实验程序与缺血／再灌注组相同，平衡15min后和再灌注期间灌流使用含2mmol／LEP的K—H液。检测心肌丙二醛（MDA）含量，分别以缺口末端标记法（TUNEL法）及免疫组化法检测心肌细胞凋亡指数（AI）及Bcl-2、Bax蛋白表达的变化。结果缺血／再灌注组MDA含量，AI和Bcl-2、Bax蛋白表达水平均明显高于对照组（均P〈0．05）；与缺血／再灌注组比较，EP组MDA含量，AI与Bax蛋白表达水平均下降，而Bcl-2蛋白表达水平显著增高（均P〈0．05）。结论EP可抑制缺血／再灌注后心肌细胞凋亡，此作用可能与其减轻氧化应激、上调Bcl-2和下调Bax蛋白表达水平有关。
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| 关 键 词： | 丙酮酸乙酯 心肌再灌注损伤 细胞凋亡 Bcl-2蛋白 Bax蛋白 |
| 修稿时间： | 2006-03-30 |
Effects of Ethyl Pyruvate on Myocardial Apoptosis and Expression of Bcl-2 and Bax Protein in Ischemia-reperfusion Rats |
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| Guo Jialong,Zhang Kailun,Jiang Xionggang et al. Effects of Ethyl Pyruvate on Myocardial Apoptosis and Expression of Bcl-2 and Bax Protein in Ischemia-reperfusion Rats[J]. Journal of Huazhong University of Science and Technology(Health Sciences), 2007, 36(2): 262-264 |
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| Authors: | Guo Jialong Zhang Kailun Jiang Xionggang et al |
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| Affiliation: | Guo Jialong,Zhang Kailun,Jiang Xionggang et al Department of Cardiovascular Surgery,Union Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430022 |
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| Abstract: | Objective To study the effects of ethyl pyruvate on cardiomyocyte apoptosis following ischemia-reperfusion(IR) in vitro and the expression of Bcl-2 and Bax proteins.Methods Isolated rat hearts were perfused in a Langendorff model.Twenty-four rats were randomly divided into 3 groups(n=8 in each group):In normal group the rats were perfused for 90 min;In I/R group,after 30 min stabilization the injury was induced by 30 min global ischemia followed by 30 min reperfusion;In ethyl pyruvate(EP) group the rats were subjected to the same protocol as the I/R group and supplied with 2 mmol/L EP 15 min before ischemia and throughout reperfusion.Myocardial malonaldehyde(MDA) content was measured.Myocardial apoptotic index(AI) was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL) method.The expression of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax in cardiac myocytes was detected by immunohistochemistry method.Results Compared with control group,the content of MDA,AI and the expression of Bcl-2,Bax proteins were increased significantly in I/R group;but as compared with control group,the content of MDA,AI and the expression of Bax protein were decreased obviously and the expression of Bcl-2 protein was up-regulated in EP group(P<0.05).Conclusion EP can inhibit cardiac myocytes apoptosis probably by alleviating oxidative stress,up-regulating Bcl-2 and down-regulating Bax proteins. |
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| Keywords: | ethyl pyruvate myocardial reperfusion injury apoptosis Bcl-2 protein Bax protein |
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