RISK信号转导通路对肠系膜上动脉缺血后处理的心肌保护作用(英文)  

RISK AND CARDIOPROTECTION OF SUPERIOR MESENTERIC ARTERY ISCHEMIC POSTCONDITIONING

作　　者：纪阳[1] 蔡尚郎[1] 徐传金[1] 

机构地区：[1]青岛大学医学院附属医院心内科,山东青岛266003

出　　处：《青岛大学医学院学报》2008年第2期129-132,共4页Acta Academiae Medicinae Qingdao Universitatis

摘　　要：目的通过在体兔心肌缺血再灌注模型，研究再灌注损伤补救酶（reperfusion injury salvage kinase，RISK）信号转导通路是否参与肠系膜上动脉缺血后处理对急性心肌缺血再灌注损伤的保护作用。方法32只兔随机分为缺血再灌注组（IR组），肠系膜上动脉缺血后处理组（MI-Post C组），缺血预处理＋肠系膜上动脉缺血后处理组（IPC＋MIPostC组），药物干预＋肠系膜上动脉缺血后处理组（DI＋MI—PostC组），每组8只。实验达终点时，取结扎血管支配部位心肌测定心肌梗死面积并观察心肌细胞超微结构改变；利用Western—blot技术检测各组动物心肌蛋白激酶B（Akt）、内皮型一氧化氮合酶（eNOS）蛋白磷酸化的表达。结果MI—PostC组和IPC＋MI—PostC组坏死面积占总面积之比均明显低于其他组（F=4．72，q=3．69～4．20，P〈0．05）；而二者之间相比，坏死面积占总面积之比无明显差别（P〉0．05）；DI＋MI—PostC组LY294002消除了缺血后处理的上述减少心肌梗死面积的作用（q=4．18，P〈0．05）。MI-PostC组Akt和eNOS蛋白表达明显高于IR和DI＋MI—PostC组（F=276．34、31．8，q=9．02～29．82，P〈0．01）；DI＋MI—PostC组LY294002消除了缺血后处理减轻再灌注损伤作用。结论心肌缺血再灌注时立即行肠系膜上动脉缺血后处理与心肌缺血预处理共同运用并不能产生额外的心脏保护作用；RISK信号转导通路参与肠系膜上动脉缺血后处理对急性心肌缺血再灌注损伤的保护作用。Objective To study whether the reperfusion injury salvage kinase （RISK） pathway take part in cardioprotection of superior mesenteric artery ischemic postconditioning on rabbit cardiac ischemia-reperfusion model in vivo. Methods The rabbits were randomly divided into the following group （eight in each group） ： Ischemia reperfusion （IR） ; superior mesenteric ar tery ischemic postconditioning （MI-PostC） ; ischemic preconditioning （IPC） ＋ MI PostC; drug intervention （DI） ＋ MI-PostC. When the experiment completed, the heart in each group was harvested and dyed with NBT （nitroblue tetrazolium）, the infarct size determined. The tissue structures were observed microscopically. Myocardium Akt and eNOS were tested by Western-blot methods. Results Infarct size was significantly less in the MI-PostC and IPC＋ MI-PostC groups than that of the other groups （F= 4.72,q= 3.69-4.20, P（0.05）, but there were no differences between this two groups. However, in DI ＋MI-PostC groups, LY294002 abrogated the myocardium infarct size reduction in MI-PostC group （q= 4.18, P（0.05）. The quantity of Akt and eNOS in myocardium was higher in MI-PostC than in the other groups （F=276.34,31.8;q=9.02-29.82;P（0.01）. Similarly,in DI ＋ MI-PostC group, LY294002 abolished this protective effect in MI-PostC group. Conclusion When reperfusion is done for the ischemic myocardium, superior mesenteric artery ischemic postconditioning can not produce supernumerary protection on the base of ischemic preconditioning. RISK pathway takes part in cardioprotection of superior mesenteric artery ischemic postconditioning.

关 键 词：心肌 缺血后处理 RISK信号转导通路 再灌注损伤 肠系膜上动脉 

分 类 号：R363[医药卫生—病理学]