Objective To explore the possible mechanism of Shenge Powder（ 参蛤散） in treating heart failure.Methods Forty-eight Wistar rats were randomized into the sham operation group

the model group

the Shenge Powder group

and the bisoprolol group（ n = 12）. Rats in other groups were built heart failure rat models by abdominal aorta constriction except the sham operation group. Five days after modeling

the Shenge Powder group was given1. 89 g/（ kg·d） of Shenge Powder suspension by gavage. The bisoprolol group was given 1 mg/（ kg·d） of bisoprolol fumarate suspension by gavage. The sham operation group and the model group were given 2. 5 ml/d of normal saline by gavage. Treatment for each of groups lasted for 12 weeks. The serum levels of lactic acid

pyroracemic acid and free fatty acid

as well as the mRNA expressions of peroxisome proliferator activated receptorγcoactivator 1α（ PGC-1α）

nuclear respiratory factor 1（ NRF1）

mitochondrial transcription factor A（ TFAM） and mitochondrial complex subunit（ including COX1

COX2

COX3

ATP6 and ATP8） in heart tissue in all groups were compared. Results The serum levels of lactic acid

pyroracemic acid and free fatty acid in the model group were higher

and mRNA expressions of heart COX1

COX2

COX3

ATP6 and ATP8 lower than those in the sham operation group;（ P < 0. 05 or P < 0. 01）. Compared with the model group

the serum level of pyroracemic acid and free fatty acid decreased

but mRNA expressions of COX2

ATP6 and ATP8 increased in the Shenge Powder group（ P < 0. 05 or P < 0. 01）.mRNA expressions of PGC-1α

NRF1 and TFAM in rats’ heart increased in the model group

the Shenge Powder group and the bisoprolol group compared with that in the sham operation group

while there was no significant difference among the three groups（ P > 0. 05）. Conclusion Shenge Powder might reduce serum metabolites accumulation by up-regulating heart mRNA expressions of COX2

ATP6 and ATP8 to protect heart mitochondrion function.