Objective To explore the possible mechanism of Xinyin Tablets（心阴片） in treating chronic heart failure（CHF）. Methods Sixty C57 BL/6 J mice were randomized into sham operation group（n=8）

model group（n=13）

trimetazidine group（n=13） and Xinyin Tablets low dose（n=13） and high dose（n=13） groups. Aortic arch constriction was carried out to prepare the model of CHF in all groups except for the sham operation group. After modeling

mice in the Xinyin Tablets low dose group and high dose group were given 292.5 mg/kg and 1170 mg/kg Xinyin Tablets by gavage

respectively; 15 mg/kg trimetazidine and 0.1 ml/10 g distilled water were administered by gavage in trimetazidine group and sham operation group

respectively; the interventions in all the groups were given to the mice once daily for eight weeks. Cardiac function indicators including left ventricular ejection fraction（LVEF）

left ventricular short axis shortening rate（LVFS）

left ventricular internal dimension diastole（LVIDd） and left ventricular internal dimension systole（LVIDs） were measured; the cardiac tissue morphology

the cardiac tissue collagen fiber deposition and the changes of myocardial cell mitochondrial ultrastructure were assessed; the protein expression of peroxisome proliferator-activated receptor γ co-activator 1α（PGC-1α）

nuclear respiration factor 1（NRF1）

and mitochondrial transcription factor B2（TFB2 M） in the cardiac tissues

as well as the myocardial tissue adenosine triphosphate（ATP） level were detected. Results Compared to the sham operation group

the model group had significantly lower levels of LVEF and LVFS

higher levels of LVIDd and LVIDs

decreased expression of PGC-1α

NRF1 and TFB2 M proteins

and decreased level of ATP in cardiac tissue（P<0.05）; the myocardial cells were significantly increased with irregular arrangement; the deposition of collagen fibers obviously increased; the number of mitochondria significantly decreased with swollen volume; the mitochondrial membrane structure was incomplete

and the cristae was blurred. Compared to those of the model group

the levels of LVEF

LVFS and LVIDs in the trimetazidine group and Xinyin Tablets low dose and high dose groups were improved

and the ATP level was significantly increased（P<0.05）; the PGC-1α and TFB2 M protein expression in Xinyin Tablets low dose group

the PGC-1α

NRF1 and TFB2 M protein expression in the Xinyin Tablets high dosegroup

and the NRF1 and TFB2 M protein expression in the trimetazidine group were significantly increased（P<0.05）; the cardiac tissue morphology in each group was significantly improved; the deposition of collagen fibers was reduced; and the ultrastructure of mitochondria was less damaged. Conclusion Xinyin Tablets may improve the cardiac function in the mice of CHF through regulating the PGC-1α/NRF1/TFB2 M signaling pathway and further promoting mitochondrial energy metabolism.