Abstract: Objective To investigate whether tetrahydrocurcumin (THC) treatment could ameliorate pressure overloadinduced cardiac hypertrophy in adult C57BL/6 mice. Methods Twenty-four C57BL/6 mice were randomly divided into four groups (n=6 in each group): the Sham, THC group, transverse aortic constriction (TAC) group, and TAC+THC group. The mice were subjected to TAC to establish the cardiac hypertrophy mouse model. The mice in the Sham and THC groups were subjected to the same procedure without ligating aortic arch. After the procedure, the mice were administered with THC (120 mg·kg-1·d-1) through drinking water. Four weeks after TAC surgery, the heart function was detected in mice. The ratios of heart / body weight (HW / BW) and lung / body weight (LW / BW) were calculated, and the mean cross-sectional area of cardiomyocytes was calculated by HE staining. The collagen deposition degree of heart tissue was observed by Masson staining. The protein expression levels of α -myosin heavy chain (α -MHC) and β -myosin heavy chain (β -MHC) were detected by Western blot assay. The expression of atrial natriuretic peptide (ANP) mRNA was detected by real-time PCR(RT-PCR). Results Four weeks after TAC surgery, the mice were presented with symptoms of cardiac hypertrophy,including the increase in HW / BW, LW / BW, the mean cross-sectional area of cardiomyocytes, collagen deposition, the expression levels of β-MHC and ANP, and the decrease in cardiac function and α-MHC expression. Compared with the TAC group, THC treatment could significantly ameliorate pathological cardiac hypertrophy caused by TAC, improve cardiac function, increase α-MHC expression, and decrease HW/BW, LW/BW, the mean cross-sectional area of cardiomyocytes,collagen deposition and the expression levels of β-MHC and ANP (P＜0.05). Conclusion THC treatment could effectively attenuate pressure overload-induced pathological cardiac hypertrophy.

Key words: hypertrophy, left ventricular, myocardium, fibrosis, curcumin, mice, inbred C57BL, tetrahydrocurcumin