丁苯酞抑制大鼠急性心肌缺血导致的心肌损伤  

Dl-3-n-butylphthalide inhibits myocardial infarction in acute myocardial ischemia

作　　者：孙明[1] 褚俊[1] 朱红军[1] 

机构地区：[1]安徽医科大学附属省立医院心血管内科,合肥230001

出　　处：《安徽医科大学学报》2014年第9期1206-1209,共4页Acta Universitatis Medicinalis Anhui

基　　金：安徽省卫生厅医学科研课题(编号:09A091;13zc006)

摘　　要：目的探讨丁苯酞(NBP)在大鼠心肌梗死后对心肌细胞线粒体损伤、心肌梗死面积及心肌细胞凋亡的作用。方法92只雄性SD大鼠分为假手术组8只,模型组、NBP低剂量组、中剂量组和高剂量组各21只。其中模型组和NBP组通过结扎冠状动脉左前降支建立急性心肌梗死模型,假手术组仅开胸,不结扎冠状动脉。采用TUNEL法检测模型组和NBP低、中、高剂量组大鼠梗死区心肌细胞凋亡。电子透射显微镜观察模型组和NBP高剂量组梗死交界区的心肌细胞超微结构。TTC染色分析模型组和NBP高剂量组心肌梗死面积,Western blot法检测模型组和NBP高剂量组大鼠心肌梗死4 h后抗凋亡蛋白Bcl-2和促凋亡蛋白Bax的表达水平。结果在大鼠急性心肌梗死实验过程中,NBP预处理过的大鼠与模型组相比,NBP中、高剂量组显著减少心肌细胞凋亡(P<0.05);NBP高剂量组可显著缩小大鼠急性心肌梗死面积(P<0.01),同时可有效抑制线粒体损伤(P<0.05);NBP高剂量组可显著提高Bcl-2蛋白表达水平(P<0.05)及Bcl-2/Bax的比值(P<0.05)。结论 NBP通过提高Bcl-2蛋白表达水平及Bcl-2/Bax的比值,减少线粒体损伤,降低心肌梗死过程中细胞凋亡指数,缩小心肌梗死面积,有效地抑制急性心肌缺血导致的心肌损伤。Objective To observe the effects of D1-3-n-butylphthalide （NBP） on the mitochondria infarction, size of myocardial infarction and myocardial apoptosis after acute myocardial ischemia in rats. Methods 92 male SD rats were divided into sham operation group （8 rats）, model group （21 rats）, and low-dose NBP group （21 rats）, medium-dose NBP group （21 rats）, high-dose NBP group （21 rats）. The model and NBP groups were made into MI model by ligation of the left anterior descending （LAD） coronary artery, but not in sham-operated group. Model group and NBP group were taken heart specimens after coronary artery ligation. Cardiomyocyte apoptosis was ana- lyzed by TUNEL in each group. Size of MI was analyzed by TI＇C staining in sham-operated group, model group and high-dose NBP group. Electron perspective microscopy was applicated in observing mitochondria infarction in model group and high-dose NBP group after myocardial infarction. The expressions of Bcl-2 protein and Bax protein were detected by Western blot. Results Compared with model group, butylphthalide significantly increased expression of Bcl-2 protein （ P 〈 0. 05 ） and the ratio of Bcl-2/Bax （ P 〈 0. 05 ）, inhibited mitochondria infarction （ P 〈 0. 05）, reduced myocardial infarct size （P 〈 0. 01 ） and cardiomyocyte apoptosis （ P 〈 O. 05 ）. Conclusion Bu- tylphthalide significantly inhibits myocardial infarction by increasing expression of Bcl-2 protein and the ratio of Bcl- 2/Bax and decreasing mitochondria infarction, reducing myocardial infarct size and cardiomyocyte apoptosis in rats during the acute myocardial ischemia process.

关 键 词：丁苯酞 冠状动脉结扎 线粒体损伤 凋亡指数 心 肌梗死 

分 类 号：R541[医药卫生—心血管疾病] R541.41[医药卫生—内科学]