AMPK信号通路调控的自噬在七氟烷后处理保护大鼠心肌缺血再灌注损伤中的机制研究

发布时间：2019-03-11 08:14

【摘要】：研究七氟烷后处理对在体大鼠心肌缺血再灌注(I/R)损伤的保护作用,探讨腺苷酸活化蛋白激酶(AMPK)介导的自噬流在七氟烷后处理心肌保护中的作用。成年雄性SD大鼠50只,建立急性大鼠在体心肌I/R损伤模型。随机分为5组:假手术组(Sham组)、缺血再灌注组(I/R组)、七氟烷后处理组(SP组)、Compound c溶剂二甲基亚砜组(DMSO组)、AMPK抑制剂Compound c组(Com c组)。除Sham组,其余各组缺血30 min,再灌注4 h末。再灌注4 h末,提取心脏,采用氯化三苯基四氮唑染色法(TTC法)测定心肌梗死范围。采用免疫印迹法(Western blot技术)检测p-AMPK/t-AMPK、LC3Ⅱ/Ⅰ及P62蛋白表达水平。与I/R组比较,SP组心肌梗死范围减小,p-AMPK/t-AMPK蛋白表达上调而LC3Ⅱ/Ⅰ、P62蛋白表达下调(P0.05);与SP组比较,Com c组心肌梗死范围增加,p-AMPK/t-AMPK蛋白表达下调而LC3Ⅱ/Ⅰ、P62蛋白表达上调(P0.05)。DMSO组相比于SP组差别无统计学意义(P0.05)。七氟烷后处理减轻了在体大鼠心肌I/R损伤,其机制可能是通过激活AMPK信号通路,减少再灌注期间自噬体的蓄积,保护自噬流进而发挥保护作用。
[Abstract]:To investigate the protective effect of sevoflurane post-treatment on myocardial ischemia-reperfusion (I-R) injury in rats, and to explore the role of adenylate-activated protein kinase (AMPK)-mediated autophagy flow in myocardial protection after sevoflurane treatment. Acute myocardial I R injury model was established in 50 adult male SD rats. They were randomly divided into 5 groups: sham-operation group (Sham group), ischemia-reperfusion group (I-R group) and sevoflurane post-treatment group (SP group), Compound c solvent dimethyl sulfoxide group (DMSO group), AMPK inhibitor Compound c (Com c group). With the exception of Sham group, the other groups were subjected to ischemia for 30 min, at the end of 4 h. At the end of 4 h reperfusion, the heart was extracted and the infarct size was measured by TTC method. The expression levels of pAMPK, LC3 鈪，

本文编号：2438113