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目的:研究黄芪甲苷(astragaloside IV)对大鼠心肌纤维化的影响和作用机制。方法:异丙肾上腺素腹腔注射造成心肌纤维化模型。大高鼠随机分为空白对照组、异丙肾上腺素模型组(10mg/kg)、异丙肾上腺素+普萘洛尔组(40mg/kg)、异丙肾上腺素+黄芪甲苷组(40mg/kg);30天后处死大鼠,分别测量大鼠全心质量指数HMI和左心室质量指数LVMI,进行组织形态学染色,测定血清中Ⅰ型前胶原羧基端前肽(PⅠCP)及其抑制物Ⅰ型胶原交联羧基末端肽(ⅠCTP);分别检测转化生长因子β(transforming growth factorβ1,TGF-β1)、Smad2/3、Smad4、Smad7、肌动蛋白α(α-SMA)的表达。结果:异丙肾上腺素模型组的HMI、LVMI较空白组明显增加;血清中PⅠCP、ⅠCTP含量增高;TGF-β1、Smad2/3、Smad 4、α-SMA含量增高,Smad7含量减少。与模型组相比,黄芪甲苷(40mg/kg)能明显降低HMI及LVMI的比例,降低TGF-β1、Smad2/3、Smad 4、α-SMA含量,Smad7含量增加,PⅠCP、ⅠCTP含量降低。结论:黄芪甲苷对异丙肾上腺素所致的大鼠心肌纤维化有保护作用,可能与黄芪甲苷能降低TGF-β1以及α-SMA产生、能够抑制TGF-βSmad通路有关。
Objective: To investigate the effect and mechanism of astragaloside IV on myocardial fibrosis in rats. Methods: Isoprenaline was induced by intraperitoneal injection of myocardial fibrosis. The rats were randomly divided into blank control group, isoproterenol model group (10mg / kg), isoproterenol + propranolol group (40mg / kg), isoproterenol + astragaloside group (40mg / kg). After 30 days, the rats were sacrificed and their total heart rate index (HMI) and left ventricular mass index (LVMI) were measured. Histomorphological staining was performed to determine the expression of type Ⅰ procollagen carboxyterminal propeptide (PⅠCP) and its inhibitor Ⅰ (Ⅰ CTP) was used to detect the expression of transforming growth factorβ1, Smad2 / 3, Smad4, Smad7 and actin α (α-SMA). Results: The levels of HMI and LVMI in isoproterenol model group were significantly higher than those in blank group. The levels of PⅠCP and ⅠCTP in serum were increased. The contents of TGF-β1, Smad2 / 3, Smad 4 and α-SMA were increased and the content of Smad7 was decreased. Compared with the model group, Astragaloside 40mg / kg significantly reduced the proportion of HMI and LVMI, decreased the content of TGF-β1, Smad2 / 3, Smad 4 and α-SMA, Smad7 content and PⅠCP, Ⅰ CTP content decreased. CONCLUSION: Astragaloside has a protective effect on isoproterenol-induced myocardial fibrosis in rats, which may be related to the decrease of TGF-β1 and α-SMA production and the inhibition of TGF-βSmad pathway by astragaloside IV.