Objective To observe the effects of Shenfu Yixin Granules（参附益心颗粒）（SFYX） on the myocardial fibrosis of rats with post-infarction heart failure（HF） and to explore the possible mechanism. Methods A model of myocardial infarction was prepared by ligating the left anterior descending coronary artery of rats. The 32 successfully modeled rats were randomly divided into a model group

a normal dose SFYX group

a high dose SFYX group and a losartan group. A sham operation group that was only threaded but not ligated was set

with 8 rats in each group. The normal dose SFYXgroup and the high dose SFYX group were given the corresponding drugs by gavage at 1.76 and 8.8 g/（kg·d）

and the losartan group was given losartan tablets at 10 mg/（kg·d） by gavage. The sham operation group and the model group were given by gavage with distilled water at 1 ml/（100 g·d）. Cardiac function was evaluated by echocardiography after 4 weeks

and left ventricular weight index（LVWI） was calculated. The distribution and content of myocardial collagen were determined by Masson staining and hydroxyproline assay. Myocardial transformation growth factor β1（TGF-β1）

Smad 2 and Smad 3 protein expression levels were determined by wstern blot; RT-PCR method was used to detect miR-21 and transforming growth factor β type Ⅲ receptor（TGF-βRⅢ） mRNA expression levels. Results Compared with the model group

left ventricular end systolic diameter（LVESD） was decreased

left ventricular ejection fraction（LVEF） and left ventricular fraction shortening（LVFS） were significantly increased

and LVMI and collagen contents were decreased

and also TGF-β1

Smad3 protein expression and miR-21 gene expression levels were depressed

while TGF-βRⅢ was increased in the normal dose of SFYX group

the high dose of SFYX group

and the losartan group（P<0.05 or P<0.01）. Conclusion SFYX can attenuate myocardial fibrosis

inhibit ventricular remodeling and improve cardiac function in rats with HF

whose mechanism might be related with regulating miR-21 so as to inhibit the excessive activation of TGF-β1/Smads signaling pathway.