Objective To explore the possible mechanism of Qiangxin Decoction（强心汤） in the treatment of chronic heart failure. Methods Fifty SD rats were randomly divided into sham operation group

model group

overlapping metalloproteinase associated protein 1（OMA1） blocking group

Qiangxin Decoction group

and the combination of OMA1 blocking and Qiangxin Decoction group

with 10 rats in each group. The left anterior descending coronary artery was ligated to establish a chronic heart failure model in rats of all groups except for sham operation group. Before establishing the model

the OMA1 group and the combination group injected 2×10

10

pfu OMA1 interference adenovirus to the rats′ tail veins to block the expression of OMA1. From the second day after the modelling

Qiangxin Decoction was administered by gavage in Qiangxin Decoction group and the combination group

with 1.62 g/kg per time

twice daily

while normal saline was administered in other groups by gavage

2 ml per time

twice daily. The heart function was measured 14 days after intragastric administration

including left ventricular end-diastolic diameter（LVDD）

left ventricular end-systolic diameter（LVDS）

and ejection fraction（EF）; RT-PCR and immunohistochemistry were used to detect the mRNA expression of OMA1 and optic atrophin 1（OPA1） in myocardial tissue

as well as the protein expression of OMA1

OPA1

long form of optic atrophy 1（L-OPA1）

and short form of optic atrophy 1（S-OPA1）; transmission electron microscope was used to observe the mitochondrial morphology in myocardial tissue. Results Compared to sham operation group

the LVDD and LVDS levels in the model group increased; the EF level decreased; the mRNA expression of OMA1 and the protein expression of OMA1 and S-OPA1 increased; the mRNA expression of OPA1 and the protein expression of OPA1 and L-OPA1 decreased（P

<

0.005）; severe edema could be seen in the mitochondria; most of the mitochondrial plates had irregular forms; paler intramembranous matrix

as well as crista fragmentation and disappearance were found. Compared to model group

the above measurements were all improved in three intervention groups

with most improvements in the combination group followed by OMA1 group and Qiangxin Decoction group（P

<

0.05）. Conclusion Qiangxin Decoction can help protect mitochondrial morphology and improve heart function

through inhibiting the expression of OMA1

reducing the proteolysis of OPA1

and decreasing the excessive cleavage of L-OPA1 to S-OPA1. And Qiangxin Decoction together with OMA1 blocking play a synergistic effect.