主 办:北 京 中 医 药 大 学
ISSN 1006-2157 CN 11-3574/R

JOURNAL OF BEIJIGN UNIVERSITY OF TRADITIONAL CHINE ›› 2017, Vol. 40 ›› Issue (1): 41-47.doi: 10.3969/j.issn.1006-2157.2017.01.009

Previous Articles     Next Articles

Effect of Qili Qiangxin Capsule on myocardial fibrosis and TGF-β1/Smad3 signaling pathway in rats with myocardial infarction*

HAN Anbang1,2, ZHANG Jian3, LU Yingdong1, ZHAO Mingjing4, ZHAO Yizhou4, HE Yaoyao2, CUI Xiangning1#   

  1. 1 Guang′anmen Hospital, China Academy of Chinese Medical Sciences, Beijing 100053;
    2 Beijing University of Chinese Medicine;
    3 Naton Medical Co.Ltd., Beijing;
    4 Dongzhimen Hospital, Beijing University of Chinese Medicine
  • Received:2016-09-02 Online:2017-01-30 Published:2017-01-30

Abstract: Objective To study the effect and mechanism of Qili Qiangxin Capsule (QQC) on myocardial fibrosis of rats with myocardial infarction(MI). Methods Acute myocardial infarction (AMI) model was induced by ligation of the proximal left anterior descending branch of coronary artery of SD male rats for four weeks. Then the survival rats with AMI were randomly divided into model group (n=12) or QQC group (n=9) according to the transthoracic echocardiography results, and 10 more rats were assigned into sham operation group. Rats of QQF group were intragastrically administered QQC at the dose of 1 g/kg once daily, while those of the other two groups took the same volume of distilled water, for consecutive four weeks. The cardiac function was measured using echocardiography, the myocardial tissue close to infarction was observed with HE or Masson staining, α-SMA expression in myocardial tissue was detected using immunohistochemistrical method, and protein expression of α-SMA, collagen I, transforming growth factor-β1(TGF-β1) and p-Smad3 were detected using Western blotting. Results Compared with the sham operation group, left ventricular fractional shortening (FS) and ejection fraction (EF) of model group were significantly lower (P<0.05), left ventricular end systolic diameter (LVID) and end systolic volume (ESV) increased significantly (P<0.05), myocardial fibrosis ratio was significantly higher (P<0.05), and the protein expression of α-SMA, collagenⅠ,TGF-β1 and p-Smad3 were higher(P<0.05). Compared with model group, EF and FS of QQF group were significantly lower (P<0.05), LVID and ESV were significantly higher(P<0.05), the degree of myocardial fibrosis was relieved, and α-SMA, collagenⅠ,TGF-β1,p-Smad3 protein expressions in myocardium were lower(P<0.05). Conclusion Qili Qiangxin Capsule was demonstrated to improve the cardiac function of rats with AMI by inhibiting the process of fibrosis remodeling, and the effects may be mediated through regulating TGF-β1/ Smad3 signaling pathway.

Key words: acute myocardial infarction, myocardial fibrosis, Qili Qiangxin Capsule, TGF-β1/ Smad3 signaling pathway, rats

CLC Number: 

  • R285.5