关键词：
北五味子乙素;心肌缺血再灌注;损伤;分子机制
摘 要：
目的:观察北五味子乙素(schisandrin B,Sch B)对缺血再灌注(ischemia/reperfusion,I/R)大鼠离体心脏功能、梗死面积、乳酸脱氢酶及相关蛋白表达的影响,探讨其对I/R损伤的保护作用及分子机制。方法:Wistar大鼠50只,随机分为5组:空白对照组(CON)、缺血再灌注组(I/R)、Sch B预保护组(Sch B)、PI3K抑制剂组(I/R+Sch B+LY)、腺苷酸活化的蛋白激酶(AMP-activated protein kinase,AMPK)抑制剂组(I/R+Sch B+CC)。采用Langendorff法建立离体大鼠心脏I/R模型,心肌缺血2 h,再灌注5、15、30、60 min。观察I/R期间室内压最大上升速率(+dp/dtmax)、室内压最大下降速率(-dp/dtmax)、左心室舒张末压、冠脉流量和心率;测定心脏灌流液中乳酸脱氢酶(lactate dehydrogenase,LDH)含量,2,3,5-氯化三苯基四氮唑(2,3,5-triphenyltertrazolium chloride,TTC)染色测定各组心肌梗死面积;免疫印迹检测心肌中总蛋白激酶B(protein kinase B,PKB)、磷酸化Akt(p-Akt)、总糖原合成酶激酶-3β(glycogen synthease kinase-3β,GSK-3β)、磷酸化GSK-3β(p-GSK-3β)蛋白表达。结果:Sch B可显著改善I/R所致的心肌功能损伤,减少梗死面积,提高心肌中p-Akt和p-GSK-3β蛋白表达。结论:Sch B对大鼠离体心脏I/R损伤具有一定保护作用,其机制可能与激活AMPK和PI3K/Akt信号通路有关。
译 名：
Protective Effect of Schisandrin B on the Isolated Rat Heart against Myocardial Ischemia/Reperfusion Injury and Its Molecular Mechanism
作 者：
SUN Hongxia;CHEN Jianguang;Pharmaceutical College, Beihua University;
关键词：
schisandrin B;;myocardial ischemia/reperfusion;;injury;;molecular mechanism
摘 要：
Objective: To observe the effect of schisandrin B(Sch B) on cardiac function, infarct size, lactate dehydrogenase and related protein expression in the isolated heart from rats with myocardial ischemia/reperfusion(I/R) injury and consequently to explore its protective effect against I/R injury and the underlying molecular mechanism. Methods: Fifty Wistar rats were randomly divided into five groups: control group(Control), ischemia/reperfusion group(I/R) and Sch B preconditioning group(Sch B), PI3 K inhibitor group(I/R + Sch B + LY294002), and AMPK inhibitor group(I/R + Sch B + Compound C). The Langendorff method was used to establish the isolated rat heart model of I/R injury, ischemia for 2 h, reperfusion for 5, 15, 30 and 60 min respectively. The +dp/dtmax,-dp/dtmax, left ventricular end-diastolic pressure(LVEDP), coronary flow(CF), heart rate(HR) and LDH activity in perfusion fluids were observed during I/R period. The myocardial infarct area was measured with TTC staining and myocardial total Akt, phosphorylation Akt, total GSK-3β and phosphorylation GSK-3β protein expression were evaluated by the Western blotting technique. Results: Sch B significantly improved the myocardial damage caused by I/R injury, reduced infarct size, and increased the expression of p-Akt and p-GSK-3β. Conclusion: Sch B has protective effects against I/R damage in isolated hearts from rats, which may be related to the activation of the AMPK and PI3K/Akt signaling pathways.
