Objective:To determine the protective effects and molecular mechanisms of asiatic acid (AA) on postoperative cardiac hypertrophy induced by transverse aortic constriction in mice. Methods:Transverse aortic constriction (TAC) was performed to establish the mice model of myocardial hypertrophy. C57BL/6 mice were divided into five groups:the Sham group,the TAC group,the TAC+AA1[25 mg/(kg-day)] group;the TAC+AA2 [50 mg/(kg-day)] group and the TAC+AA3 [100 mg/(kg-day)] group. After 2 weeks of TAC,echocardiography was performed to measure the hypertrophic criteria of the hearts. The protein expressions of TGF-β1,p-p38,p38,p-ERK1/2 and ERK1/2 were detected by Western blot. The mRNA expressions of ANP and TGF-β1 were detected by real-time PCR. Results:AA significantly inhibited cardiac hypertrophy induced by TAC,improved cardiac function,reduced the mRNA and protein expression of TGF-β1,as well as the phosphorylation of p38 and ERK1/2. Conclusion:AA attenuates TAC-induced cardiac hypertrophy. The protective mechanisms of AA may through inhibiting TGF-β1-p38/ERK1/2 signaling pathway.