PI3K/Akt通路介导Apelin后处理减轻离体大鼠心脏缺血再灌注损伤

【目的】 探讨Apelin后处理对离体大鼠心脏缺血再灌注损伤的影响及其信号机制.【方法】 32只SD大鼠随机分为4组,每组8只:缺血再灌注对照组、Apelin后处理组、Apelin后处理加渥曼青霉素(磷脂酰肌醇-3激酶抑制剂)处理组、渥曼青霉素处理对照组,观察Apelin后处理对大鼠离体缺血再灌注心脏左心室收缩压、心率、冠状动脉流量、肌酸磷酸激酶和乳酸脱氢酶释放以及左室心肌蛋白激酶B(Akt)磷酸化的影响.【结果】 与缺血再灌注对照组相比,Apelin后处理组心脏左心室收缩压、心率和冠状动脉流量得到改善,释放到冠状动脉循环流出液中的肌酸磷酸激酶,乳酸脱氢酶量减少,同时左室心肌磷酸化Akt(Ser473)水平增高;而渥曼青霉素抑制了Apelin后处理所致的Akt磷酸化,并完全消除了Apelin后处理的心脏保护作用.【结论】 Apelin后处理能够减轻离体大鼠心脏缺血再灌注损伤,PI3K/Akt信号通路参与介导Apelin后处理的心脏保护作用.

Apelin Postconditioning Attenuates Isolated Rat Heart Ischemia Reperfusion Injury through PI3K/Akt Signaling Pathway

【Objective】 To explore the effects of apelin postconditioning on isolated rat heart ischemia reperfusion injury and investigate the underlying signal mechanism. 【Methods】 Thirty-two rats were randomized to 4 groups: ischemia reperfusion (IR) control group, IR treated with apelin postconditioning group, IR treated with apelin postconditioning and phosphatidylinositol-3-kinase (PI3K) inhibitor wortmannin group, and IR treated with wortmannin alone to evaluate the effects of apelin postconditioning on left ventricular systole pressure, coronary artery flow, creatine phosphokinase (CK) and lactate dehydrogenase (LDH) release, and the level of myocardial phospho-protein kinase B/Akt (Ser473). 【Results】 Left ventricular systole pressure, heart rate, and coronary artery flow were improved significantly, and the release of CK and LDH was reduced significantly in apelin postconditioning group as compared to ischemia reperfusion control group. Moreover, the levels of phospho-protein kinase B/Akt (Ser473) was increased in apelin postconditioning group compared with ischemia reperfusion control group. Wortmannin inhibited the increase of phospho-protein kinase B/Akt (Ser473) induced by apelin postconditioning, and abolished the cardioprotection of apelin postconditioning. 【Conclusion】 Apelin postconditioning attenuates isolated rat heart ischemia reperfusion injury. The PI3K/Akt signal pathway is involved in the cardioprotection of apelin postconditioning.