中文摘要：

Hyperlipidemia 是在 ischemic 心疾病的发展的一个独立风险因素，它能增加心肌的危险性到 ischemia/reperfusion (I/R ) 损害。Ischemic postconditioning (PostC ) 现在作为新奇策略被表明了处于正常条件对心肌的 I/R 损害利用自然的保护。然而， hyperlipidemic 动物上的 PostC 的效果留下逃犯。PostC 减少心肌的 I/R 损害，这在我们的以前的学习被显示出，并且组织缺氧可诱导的 factor-1 (HIF-1 ) 可以在正常老鼠上在 PostC 的 cardioprotective 机制起一个重要作用。这里，我们测试了 hyperlipidemic 老鼠上的 PostC 的 cardioprotection 与起来调整的 HIF-1 表示被联系的假设。男 Wistar 老鼠用一本高脂肪的食谱被喂 8 个星期，然后随机把组划分了成五：假冒， I/R， dimethyloxalylglycine (DMOG )+ I/R， PostC，和 DMOG + PostC 组织。I/R 损害导致的有害索引包括了梗塞尺寸，血浆肌酸 kinase (CK ) 活动和 caspase-3 活动。，结果与 I/R 组相比证明 PostC 能减少梗塞尺寸，它与血浆 CK 的重要底层一致活动和 caspase-3 活动，和那它在 hyperlipidemic 老鼠增加了 HIF-1 的表示。当 DMOG 在 PostC 前被给起来调整 HIF-1 蛋白质水平时， I/R 损害的度被稀释。在结论，这些数据建议 HIF-1 的起来规定可以是对在 hyperlipidemic 老鼠的 I/R 损害的 PostC 的 cardioprotective 机制之一。

英文摘要：

Hyperlipidemia is an independent risk factor in the devel- opment of ischemic heart disease, which can increase myo- cardial susceptibility to ischemia/reperfusion （I/R） injury. Ischemic postconditioning （PostC） has now been demon- strated as a novel strategy to harness nature＇s protection against myocardial I/R injury in normal conditions. However, the effect of PostC on hyperlipidemic animals remains elusive. It has been shown in our previous study that PostC reduces the myocardial I/R injury, and hypoxia- inducible factor-1α （HIF-1α） may play an important role in the cardioprotective mechanisms of PostC on normal rats. Here, we tested the hypothesis that the cardioprotec- tion of PostC on hyperlipidemic rats is associated with the up-regulated HIF-1α expression. Male Wistar rats were fed with a high-fat diet for 8 weeks, and then randomly div- ided into five groups： sham, I/R, dimethyloxalylglycine （DMOG） ＋ I/R, PostC, and DMOG ＋ PostC group. The detrimental indices induced by I/R injury included infarct size, plasma creatine kinase （CK） activity and caspase-3 ac- tivity. The results showed that PostC could reduce the infarct size, when compared with the I/R group, which was consistent with the significant lower levels of plasma CK activity and caspase-3 activity, and that it increased the ex- pression of HIF-1α in hyperlipidemic rats. When DMOG was given before PostC to up-regulate HIF-1α protein level, the degree of I/R injury was attenuated. In conclu- sion, these data suggested that the up-regulation of HIF-1α may be one of the cardioprotective mechanisms of PostC against I/R injury in hyperlipidemic rats.