Objective To investigate the possible mechanism of Qidan Lixin Pill（ 芪丹利心丸） in prevention and treatment of myocardial fibrosis after myocardial infarction. Methods Rat models of myocardial infarction were established by permanent left coronary artery ligation and were randomly divided into model group

captopril group and Qidan Lixin Pill group

and a sham-operation group was threaded without ligating

with 10 rats in each group. On the second day after surgery rats were administered intragastrically for 4 weeks

and Qidan Lixin Pill group was given Qidan Lixin Pill 2. 43 g/（ kg · d）

captopril group given captopril tablet 2. 25 mg/（ kg · d）

and the other groups given 10 ml/（ kg·d） of deionized water for intragastric administration. After 4 weeks

the cardiac hemodynamics indicators including heart rate（ HR）

left ventricular systolic pressure（ LVSP）

left ventricular end-diastolic pressure（ LVEDP）

maximum rate of increase in left ventricular pressure（ + dp/dt max）

maximum rate of decrease in left ventricular pressure（-dp/dt max） were detected. The left ventricular mass（ LVM） was weighed

the left ventricular mass index（ LVMI） calculated

and HE staining was used for pathological observation while Masson staining was used to calculate collagen volume fraction（ CVF）. The miR-133 a

the expressions of mRNA and protein of transforming growth factor-β1（ TGF-β1） and connective tissue growth factor（ CTGF） in each group were detected.Results Compared with sham-operation group

the LVSP and + dp/dt max

-dp/dt max in model group were decreased while LVEDP was increased

LVMI and CVF increased

miR-133 a decreased

and the expressions of mRNA and TGF-β1 and CTGF protein were increased（ P < 0. 01）. Compared with the model group

the LVSP and + dp/dt max

-dp/dt max in Qidan Lixin Pill group were increased while LVEDP was decreased

LVMI and CVF decreased

miR-133 a increased

and the expressions of mRNA and TGF-β1 and CTGF protein were decreased（ P < 0. 05 or P <0. 01）. The HE staining results showed that the residual myocardial fibers were disordered and partly fractured

and the muscle space was widened obviously in model group. The myocardial fibers in the peripheral areas of myocardial infarction were relatively regular in shape

and most of the cell membranes were basically complete in both captopril group and Qidan Lixin Pill group. Conclusion Qidan Lixin Pill can prevent myocardial fibrosis in rats with myocardial infarction

and the intervention mechanism may be related to miR-133 a/TGF-β1/CTGF signaling pathway.