中文摘要：

目的：观察罗布麻叶提取物（AVLE）预处理对心肌缺血再灌注（MI/R）大鼠心肌细胞凋亡和细胞信号转导系统中丝（苏）氨酸激酶（Akt）和细胞外信号调节激酶（ERK1/2）的影响。方法：采用SD大鼠MI/R模型（结扎冠脉左前降支起始部30min后再灌注4h）,随机分为Sham组（假手术）、MI/R组、AVLE预处理组[AVLE（500mg/kg）灌胃,每日一次,连续灌胃7天后再行MI/R]。用TUNEL法检测各组心肌细胞凋亡,计算凋亡指数（AI）;荧光免疫分析法检测各组心肌组织凋亡蛋白Caspase-3活性;Western Blotting测定心肌组织Akt和ERK1/2的表达水平和磷酸化水平。结果：与Sham组比较,MI/R组心肌细胞AI显著升高（P〈0.05）,心肌组织Caspase-3活性明显升高（P〈0.05）,心肌Akt和ERK1/2的磷酸化水平显著降低（P〈0.05）;与MI/R组比较,AVLE预处理组AI明显下降（P〈0.05）,心肌组织Caspase-3活性显著降低（P〈0.05）,Akt和ERK1/2磷酸化水平显著升高（P〈0.05）。结论：AVLE能够抑制缺血再灌注所致心肌细胞损伤,其作用与生存信号通路蛋白PI3K/Akt和ERK1/2的活化水平有关。

英文摘要：

Objective：To investigate the effect of apocynum venetum leaf extract （AVLE）on myocardium is-chemia reperfusion（MI/R）inj ury rat and signal pathway serine/threonine kinase （Akt）and the mitogen-activated protein kinase p42/44extra-cellular signa-l regulated kinases （ERK1/2）.Method：Male Sprague-Dawley rats were divided into 3 groups randomly：sham,ischemia reperfusion,AVLE preconditioned[（500mg/kg/d,o.g.）once dai-ly for one week]＋MI/R.The model of myocardial I/R inj ury in vivo was made by ligating the left anterior descend-ing artery for 30 min followed by 4 h of reperfusion in SD rats.Cardiomyocyte apoptosis was detected using in situ TDT-mediated dUTP nick end labeling （TUNEL）.The activity of Caspase-3 was determined by fluorescent assay. The expressions and phosphorylations of Akt and ERK1/2 were measured using Western blot.Results：Compared with Sham group,the apoptosis index and the expressions of Caspase-3 were significantly increased and the phos-phorylations of both Akt and ERK1/2 in I/R cardiac issue were significantly attenuated in MI/R group （P〈0.05）. Compared with I/R group,the apoptosis index and the expressions of Caspase-3 were significantly attenuated in AVLEpreconditioned animals （P〈0.05）.AVLE preconditioning significantly increased the phosphorylations of both Akt and ERK1/2 in I/R cardiac issue （P〈0.05）.Conclusion：The results suggest that AVLE preconditioned may be a-ble to protect the heart against reperfusion-induced inj ury mediated by the increase of phosphorylating Akt and ERK1/2.