高密度脂蛋白抗动脉粥样硬化功能的丢失与恢复

巨噬细胞在动脉粥样硬化(As)起始、发展的全过程扮演着中心角色,从巨噬细胞脂质积聚和炎症反应入手,寻求某个作用环节进行干预有可能成为非常合适的As治疗靶点。内皮功能失调是As发生的一个重要起始事件,内皮细胞释放的粘附分子如ICAM、VCAM、ELAM及Selectin,介导单核细胞活化并向内膜下募集、分化,巨噬细胞释放的单核细胞趋化蛋白1(MCP-1)及巨噬细胞移动抑制因子(MIF)在单核细胞的移行和分化中发挥重要作用。MIF还可诱导ICAM、....

The Effects of Nicorandil Postconditioning on Ischemia-Induced Cardiomyocyte Apotosis in Acute Myocardial Ischemia Rats

Aim To study the effect and possible mechanism of nicorandil postconditioning on myocardial ischemia reperfusion(MIR) injury in rats. Methods The SD rats were randomly divided into six groups: control group,ischemia reperfusion group,postconditioning group,nicorandil postconditioning groups of 2 mg/kg,5 mg/kg,and 10 mg/kg.Ischemia reperfusion group was obtained by ligated left anterior descending coronary artery 30 minutes and followed by 120 minutes reperfusion.Postconditioning group was obtained by 5 cycles of brief 10 seconds intermittent reperfusion/reocclusion.After 30 minutes ischemia,hearts were exposed to nicorandil for 10 minutes immediately at the onset of reperfusion.Contents of creatine kinase(CK) and malondialdehyde(MDA),activity of superoxide dismutase(SOD) were detected respectively.Apoptosis rates and the expression of caspase-3 were investigated. Results In the nicorandil postconditioning groups,contents of CK and MDA were lower,activities of SOD were higher,apotosis rates were decreased,and caspase-3 was lower. Conclusions Nicorandil postconditioning could protect MIR.The myocardial protective mechanism maybe realized by enhancing the activity of SOD,enhancing myocardial antioxygen capability,reducing the oxygen free radical injury,stabilizing myocardial cellular membrance and inhibition of apoptosis.