中文摘要：

目的研究红景天苷（Salidroside,SAL）对力竭运动导致大鼠心肌结构损伤和线粒体呼吸功能障碍的影响。方法将40只雄性SD大鼠随机分为对照（C）组、力竭（EE）组、低剂量SAL（LS）组、高剂量SAL（HS）组（n=10）。C组与EE组分别给予生理盐水[10 ml/（kg·d）]、其他两组给予低剂量SAL[100 mg/（kg·d）]及高剂量SAL[300mg/（kg·d）]灌胃2周。除C组外,其余各组建立一次性力竭游泳运动后心肌损伤模型,于力竭游泳运动后即刻取材,C组同时在安静状态下取材。应用光镜及电镜观察大鼠心肌显微结构及超微结构。采用原位法应用高分辨呼吸仪分别测定大鼠心肌线粒体呼吸链复合物Ⅰ、Ⅱ、Ⅳ的态3呼吸速率。结果①与C组比较,EE组大鼠心肌线粒体呼吸链复合物Ⅰ、Ⅱ、Ⅳ的态3呼吸速率明显降低（P〈0.05）;形态学观察可见心肌细胞损伤严重,心肌纤维出现断裂,间质水肿,可见畸形线粒体以及线粒体嵴有断裂。②与EE组比较,LS组大鼠心肌线粒体呼吸链复合物Ⅰ的态3呼吸速率明显增高（P〈0.05）,HS组线粒体呼吸链复合物Ⅰ、Ⅱ、Ⅳ的态3呼吸速率明显增高（P〈0.05）;形态学观察偶见肌纤维断裂、心肌细胞基质水肿,线粒体部分嵴和少部分膜融合、模糊不清或缺失。③与LS组比较,HS组线粒体呼吸链复合物Ⅰ、Ⅱ、Ⅳ的态3呼吸速率明显增高（P〈0.05）,心肌纤维的完整性好于LS组,线粒体变异程度轻,膜结构相对完整。结论 SAL对力竭运动导致大鼠心肌结构损伤和线粒体呼吸功能障碍有保护作用,且这种作用呈剂量依赖性。

英文摘要：

Objective To study the effect of Salidroside（ SAL） on myocardial structure and respiratory dysfunction of mitochondria in rats after exhaustive exercise. Methods A total of 40 healthy male Sprague Dawley（ SD） rats were randomly divided into control group（ C group,n = 10）,exhausting exercise group（ EE group,n = 10）,low-dose SAL group（ LS group,n = 10） and high-dose SAL group（ HS group,n = 10）. C and EE groups were administered with physiological saline [10 ml /（ kg·d） ] intragastrically for 2 weeks,while LS and HS groups were administered respectively with SAL [100 mg /（ kg·d） ]and SAL [300 mg /（ kg·d） ]intragastrically for 2 weeks. The models of exhausting swimming exercise were established except for control group. Myocardium samples were taken immediately after the training,while the samples were taken under resting state in the control group at the same time. Myocardial microstructure and ultrastructure were observed under light microscope and transmission electron microscope. The State 3 respiratory rates of the myocardial mitochondrial electronic transport chain complexⅠ,Ⅱ and Ⅳ were measured in situ with high-resolution respirometer. Results ①Compared with those in C group,the State 3 respiratory rates of the myocardial mitochondrial electronic transport chain complexⅠ,Ⅱ and Ⅳ in EE group were significantly decreased（ P 〈 0. 05）; histomorphology observation showed that the myocardial cells were seriously damaged,breakage and interstitial edema were found in cardiac muscle fibers,and abnormal mitochondrion and breakage crista mitochondriales were also found. ② Compared with those in EE group,the State 3 respiratory rate of the myocardial mitochondrial electronic transport chain complexⅠ was significantly improved in LS group（ P〈0. 05）; State 3 respiratory rates of complex Ⅰ,Ⅱ and Ⅳ were significantly elevated in HS group（ P〉 0. 05）; histomorphology observation showed that breakage muscle fibers and edema of myocardial cytoplasmi