Objective: To evaluate the effect of Xuanbi Antong formula (XBF) on ventricular remodeling in myocardial infarction rats and its mechanism. Method: In this study

the acute myocardial infarction model was established by ligating the anterior descending coronary artery in Wistar rats. After administration with XBF (1.22 g·kg-1·d-1) for 4 weeks

the effect of XBF on apparent signs and cardiac indexes of the Wistar rats were observed

the left ventricular ejection fraction (LVEF) observed by Doppler ultrasonography

the changes in cardiac morphology were observed by pathological examination

the expressions of tumor necrosis factor-α(TNF-α)

interleukin-6 (IL-6) and IL-10 were detected by enzyme-linked immunosorbent assay (ELISA)

and the expressions of Caspase-3 and Caspase-9 were detected by immunohistochemistry and Western blot. Result: Compared with model group

the survival conditions of rats in all treatment groups were generally improved after XBF treatment

LVEF were significantly increased (P<0.05)

both LV end-diastolic inner diameter (LVIDd) and LV end-systolic inner diameter (LVIDs) were significantly reduced (P<0.05). Pathological examination showed that the myocardium degeneration of the rats treated with XBF was decreased in a good order

the myofilaments were complete

the gaps were more uniform

and the interstitial collagen fibers were significantly reduced. The mitochondrial structure of cardiomyocytes was significantly improved

the ultrastructure was clear

and the arrangement of myofilaments was more regular. TNF-α and IL-6 were decreased (P<0.01)

and IL-10 was increased (P<0.05) in rats treated with XBF. The expressions of Caspase-3 and Caspase-9 were descended in rats treated with XBF (P<0.05). Conclusion: XBF for 'clearing heat

promoting blood circulation and removing phlegm' can significantly improve the LVEF of rats after ventricular remodeling resulted in myocardial infarction. The mechanism may be that XBF can decrease and inhibit inflammatory factors for promoting ventricular remodeling

such as TNF-α and IL-6

increase inflammatory inhibitor IL-10

and inhibit the expressions of Caspase-3 and Caspase-9.