中文摘要：

目的：探讨线粒体ATP敏感性钾离子通道（mitoKATP）开放剂二氮嗪（DE）对离体大鼠供心不同时程冷保存时促凋亡蛋白Smac／DIABLO表达的影响及机制。方法：SD大鼠随机分为3组，包括空白对照组、单纯冷保存组、DE组（Celsior保存液中含30μmol／LDE），后2组又按冷保存时程不同，分别分为3、6、9、12h组。实验结束后采用原位末端标记染色法（TUNEL）检测心肌细胞凋亡，采用Westernblotting法检测心肌组织中caspase-3蛋白及胞浆Smac／DIABLO蛋白表达。结果：（1）在Celsior保存液中加入DE后，心肌细胞凋亡指数及caspase-3蛋白表达显著低于相应单纯冷保存组。（2）DE可使Smac／DIABLO蛋白表达高峰由冷保存6h延迟至9h。（3）DE的上述作用可被mitoKATP通道特异性阻断剂5-羟基葵酸盐（5-HD）所取消。结论：DE具有对抗冷保存诱导心肌细胞凋亡的作用，这种保护作用可能与其激活mitoKATP通道和减少促凋亡蛋白Smac／DIABLO表达有关。

英文摘要：

AIM ： To investigate the effect of a mitochondrial ATP - sensitive potassium channel （ mitoKATP ） opener diazoxide （ DE ） on Srnac/DIABLO protein expressions in rat heart suffered from different duration of hypothermic preservation. METHODS ： The Langendorff model of isolated rat heart was used. After stored in 4 ℃ Celsior solution with or without DE （30 μmol/L） for different time （0, 3, 6, 9 or 12 h）. Cell apoptosis was detected by TUNEL technique. The expression of Smac/DIABLO protein in cytoplasm and total caspase - 3 protein in myocardia tissue was also anaJyzed by Western blotting. RESULTS ： （ 1 ） Compared to the hypothermic preservation groups, DE reduced the percentage of apoptotie cells and the expression of caspase -3 protein in myocardia tissue. （2） The peak of Smac/DIABLO protein expression level appeared at 6 h after hypotherrnic preservation, and which was postponed to 9 h by DE. （3） The above effects of DE were attenuated by a mitoKATP channel inhibitor 5 - hydroxydeeanoate （5 - HD）. CONCLUSION： The findings indicate that in the isolated rat heart, DE protects myocardium against different duration of hypothermic preservation injury via opening of mitoKATP channel and inhibition of Smac/DIABLO protein expression.