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目的:研究丹参注射液(丹参)对大鼠心肌缺血再灌注损伤的保护效应。方法:用在体左冠状动脉前降支穿线结扎法制备心肌缺血再灌注模型。60只 SD 大鼠分为3组,假手术组10只,缺血再灌注组25只,丹参干预组25只。缺血30min,再灌注120min。观察心肌梗死范围和心肌细胞超微结构变化,采用缺口末端标记法(TUNEL),检测心肌细胞凋亡指数(AI)。结果:丹参干预组缺血面积[(40.38±2.84)%]较缺血再灌注组[(42.32±2.28)%]缩小(P<0.05);丹参干预组梗死面积[(60.38±2.62)%]较缺血再灌注组[(65.63±1.68)%]缩小(P<0.01)。电镜下,缺血再灌注组肌纤维挛缩,核固缩,染色质浓缩,沿核膜下凝聚,线粒体嵴疏松,空泡形成;丹参干预组肌节较清晰,线粒体嵴较密集,无明显空泡形成。AI 缺血再灌注组(28.9±3.6)较假手术组(2.2±0.6)增加(P<0.01);丹参干预组(26.2±3.4)较缺血再灌注组(28.9±3.6)]下降(P<0.01)。结论:丹参能抑制心肌细胞凋亡,减少心肌细胞损伤,缩小梗死范围,达到保护心肌缺血再灌注损伤的目的。
Objective: To study the protective effect of salvia miltiorrhiza injection on myocardial ischemia-reperfusion injury in rats. METHODS: Myocardial ischemia-reperfusion model was prepared by threading ligation of the left anterior descending coronary artery. 60 SD rats were divided into 3 groups, 10 in the sham group, 25 in the ischemia-reperfusion group, and 25 in the Salvia miltiorrhiza intervention group. Ischemia 30min, reperfusion 120min. Myocardial infarct size and ultrastructural changes of myocardial cells were observed. Apoptosis index (AI) of myocardial cells was detected by nick end labeling (TUNEL). Results: The ischemic area [(40.38±2.84)%] of Danshen intervention group was smaller than that of ischemia-reperfusion group [(42.32±2.28)%] (P<0.05); the infarct size of Danshen intervention group [(60.38±2.62)%] Compared with the ischemia-reperfusion group [(65.63±1.68)%], it decreased (P<0.01). Under electron microscopy, the ischemia-reperfusion group had muscle fibers contracting, nuclear condensation, chromatin condensation, coagulation along the nucleus membrane, loose mitochondrial crista, vacuolization; Salvia miltiorrhiza intervened group had clear sarcomere, dense mitochondria, and no obvious vacuolization. form. The AI ischemia-reperfusion group (28.9±3.6) increased compared with the sham group (2.2±0.6) (P<0.01); the Danshen intervention group (26.2±3.4) decreased compared with the ischemia-reperfusion group (28.9±3.6) (P <0.01). Conclusion: Salvia miltiorrhiza can inhibit the apoptosis of cardiomyocytes, reduce the damage of myocardial cells, reduce the infarct size, and achieve the purpose of protecting myocardial ischemia-reperfusion injury.