生脉散对心衰大鼠心肌纤维化及TGF-β1/Smad3通路的影响  

Effect of Shengmaisanr on myocardial fibrosis and TGF-β1/Smad3 pathway in heart failure rats

作　　者：齐静[1] 陈韦[1] 周鑫[1] 于乐[1] 徐刚[1] 姚辉 胡楠 侯平[1] QI Jing;CHEN Wei;ZHOU Xin;YU Le;XU Gang;YAO Hui;HU Nan;HOU Ping(Department of Cardiology,Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110032;Liaoning University of Traditional Chinese Medicine,Shenyang 110032,China)

机构地区：[1]辽宁中医药大学附属医院心内科,辽宁沈阳110032 [2]辽宁中医药大学,辽宁沈阳110032

出　　处：《解剖科学进展》2020年第5期583-586,590,共5页Progress of Anatomical Sciences

基　　金：国家自然科学基金项目(81874403);辽宁省自然科学基金项目(20170540599,20180550907)。

摘　　要：目的观察生脉散对心力衰竭(心衰)大鼠心肌纤维化的作用及其作用机制。方法取SD大鼠50只,采用盐酸异丙肾上腺素(ISO)诱导法建立心衰大鼠模型,随机分成空白对照组(Control组)、心衰模型组(HF组)、生脉散低剂量组(SMS-L组)、生脉散中剂量组(SMS-M)、生脉散高剂量组(SMS-H)5组,连续给药4周,收集各组大鼠心脏结构参数,HE染色、Masson染色观察各组大鼠病理学变化,蛋白免疫印迹(Western blot)、实时荧光定量(qRT-PCR)检测各组大鼠左室心肌组织中转化生长因子(TGF)-β1/Smad3通路相关蛋白及I型胶原蛋白(collagen I)、III型胶原蛋白(collagen III)的表达情况。结果ISO导致大鼠HF模型心功能下降及心室重构,大鼠左室舒张末内径(LVDD)、左室收缩末内径(LVSD)增大,左室射血分数(LVEF)、左室短轴缩短率(LVFS)降低;心肌细胞肿胀,界线模糊不清,大量炎性细胞浸润及胶原蛋白沉积。SMS干预改善了大鼠心功能及心室重构现象,LVDD、LVDS降低,LVEF、LVFS升高;SMS-H组大鼠心肌细胞结构较为完整,仅见少量炎性细胞浸润及胶原纤维蛋白沉积现象,同时SMS下调了collagen I、collagen III、TGF-β1、p-Smad3的表达。结论生脉散能够显著改善ISO诱导心衰大鼠心功能,其作用机制可能通过调控TGF-β1/Smad3通路从而抑制心肌纤维化。Objective To observe the effect and its mechanism of Shengmaisan on myocardial fibrosis in heart failure(HF)rats.Methods 50 SD rats were selected and isoprenaline(ISO)was used to establish the rat model of heart failure.Randomly divided into 5 groups:Blank Control group(Control group),Heart failure model group(HF group),Shengmaisan low-dose group(SMS-L group),Shengmaisan medium-dose group(SMS-M),Shengmaisan high-dose group(SMS-H).The drug was administered continuously for 4 weeks.Cardiac structural parameters of each group were collected.HE staining,Masson staining to observe the pathological changes of each group of rats.Western blot and quantitative Realtime Polymerase Chain Reaction(qRT-PCR)were used to detect the expression of the related protein of transforming growth factor(TGF)-β1/Smad3 pathway,collagen I and collagen III in the left ventricular myocardial tissues of each group.Results ISO caused a decrease in cardiac function and ventricular remodeling in the rat HF model.The left ventricular end-diastolic diameter(LVDD)and left ventricular end-systolic diameter(LVSD)increased,and left ventricular ejection fraction(LVEF)and left ventricular short-axis shortening rate(LVFS)decreased.Myocardial cells were swollen,the boundaries were blurred,a large number of inflammatory cells infiltrate and collagen deposits were seen.SMS improved rat heart function and ventricular remodeling.LVDD and LVDS were reduced,and LVEF and LVFS were increased.The structure of myocardial cells in the SMS-H group was relatively complete,with only a small amount of inflammatory cell infiltration and collagen fibrin deposition.At the same time,SMS down-regulated the expression of collagen I,collagen III,TGF-β1,and p-Smad3.Conclusion Shengmaisan can significantly improve cardiac function in iso-induced heart failure rats,and its mechanism may inhibit myocardial fibrosis by regulating TGF-β1/Smad3 pathway..

关 键 词：心力衰竭 生脉散 心肌纤维化 TGF-β1/Smad3通路 

分 类 号：R541.6[医药卫生—心血管疾病]