四氢姜黄素对压力负荷引起的小鼠心肌肥厚的保护作用

目的 探究四氢姜黄素（THC）能否减轻压力负荷引起的成年小鼠病理性心肌肥厚。方法 24只C57BL/6小鼠随机分为4组：假手术（Sham）组、THC组、主动脉弓缩窄（TAC）组及TAC+THC组，每组6只。通过TAC术建立小鼠心肌肥厚模型，Sham组和THC组不结扎主动脉弓。TAC术后每日通过饮水摄入THC（120 mg/kg）。TAC术后4周检测小鼠心脏功能，分离心脏和肺脏计算心脏/体质量比和肺脏/体质量比，HE 染色计算心肌细胞平均横截面积，Masson 染色观察心脏组织胶原沉积程度，Western blotting 检测 α-肌球蛋白重链（α-MHC）、β-肌球蛋白重链（β- MHC）蛋白表达，实时定量PCR（real-time PCR）检测心房钠尿肽（ANP）mRNA表达情况。结果 TAC术后4周，小鼠发生病理性心肌肥厚，表现为心脏/体质量比、肺脏/体质量比、心肌细胞平均横截面积、心脏组织胶原沉积、β-MHC和ANP表达较Sham组小鼠明显增高，而左室射血分数（LVEF）、左室短轴缩短率（LVFS）和α-MHC表达较Sham组小鼠明显降低。与TAC组相比，THC处理可以明显缓解TAC引起的病理性心肌肥厚，改善心脏功能，提高α-MHC表达，降低心脏/体质量比、肺脏/体质量比、心肌细胞平均横截面积、心脏组织胶原沉积、β-MHC和ANP表达（均P＜ 0.05）。结论 THC能够有效减轻压力负荷引起的病理性心肌肥厚。

The protective effects of tetrahydrocurcumin on the treatment of pressure overload-induced

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.