中文摘要：

Hyperlipidemia 在 ischemic 心疾病的发展被认为是一个独立风险因素，并且它能增加心肌的危险性到 ischemia/reperfusion (I/R ) 损害。Ischemic postconditioning (Postcon ) 被表明了稀释 I/R 处于正常条件导致的心肌的损害。但是 hyperlipidemic 动物上的 ischemic Postcon 的效果是未知的。组织缺氧可诱导的 factor-1 (HIF-1 ) 被表明了由 preconditioning 在 cardioprotection 起一个中央作用，它除了 Postcon 是保护的策略之一。这研究的目的是决定 Postcon 是否能在 hyperlipidemic 动物减少心肌的损害并且估计 HIF-1 是否涉及 Postcon 机制。在用高胖的饮食或正常饮食喂了 8 个星期以后，男 Wistar 老鼠经历了左前面的下降冠的吸藏因为 30 min 由灌注的 180 min 列在后面与或没有 Postcon。I/R 侮辱导致的有害索引包括了梗塞尺寸，血浆肌酸 kinase 活动和 caspase-3 活动。结果证明 hyperlipidemia 显著地提高了 I/R 导致的心肌的损害，当 Postcon 显著地减少了时在 normolipidemic 和 hyperlipidemic 老鼠的心肌的损害。而且， hyperlipidemia 和 I/R 支持了 HIF-1 表示。最重要地，我们第一次证明了 Postcon 进一步不仅在 normolipidemic 而且处于 hyperlipidemic 条件在 HIF-1 蛋白质水平导致了重要增加。因此， Postcon 减少 I/R 在正常和 hyperlipidemic 导致的心肌的损害动物，和 HIF-1 upregulation 可以在调停 Postcon 的 cardioprotective 机制包含。

英文摘要：

Hyperlipidemia is regarded as an independent risk factor in the development of ischemic heart disease, and it can increase the myocardial susceptibility to ischemia/reperfusion （I/R） injury, lschemic postconditioning （Postcon） has been demonstrated to attenuate the myocardial injury induced by I/R in normal conditions. But the effect of ischemic Postcon on hyperlipidemic animals is unknown. Hypoxia inducible factor-1 （HIF-1） has been demonstrated to play a central role in the cardioprotection by preconditioning, which is one of the protective strategies except for Postcon. The aim of this study was to determine whether Postcon could reduce myocardial injury in hyperlipidemic animals and to assess whether HIF-1 was involved in Postcon mechanisms. Male Wistar rats underwent the left anterior descending coronary occlusion for 30 min followed by 180min of reperfusion with or without Postcon after fed with high fat diet or normal diet for 8 weeks. The detrimental indices induced by the I/R insult included infarct size, plasma creatine kinase activity and caspase-3 activity. Results showed that hyperlipidemia remarkably enhanced the myocardial injury induced by I/R, while Postcon significantly decreased the myocardial injury in both normolipidemie and hyperlipidemic rats. Moreover, both hyperlipidemia and I/R promoted the HIF-αL expression. Most importantly, we have for the first time demonstrated that Postcon further induced a significant increase in HIF-αL protein level not only in normolipidemie but also in hyperlipidemic conditions. Thus, Postcon reduces the myocardial injury induced by I/R in normal and hyperlipidemic animals, and HIF-αL upregulation may involve in the Postcon-mediated cardioprotective mechanisms.