中文摘要：

目的观察龙胆苦苷（GPS）对主动脉弓缩窄术诱导的C57BL小鼠心肌肥厚是否有预防作用。方法 40只雄性C57BL小鼠随机分成假手术组（n=8）和心肌肥厚模型组（n=32）,心肌肥厚模型组通过主动脉弓缩窄术建立心肌肥厚模型。术后24 h随机分成心肌肥厚模型组和龙胆苦苷低[2.5 mg/（kg·d）]、中[5.0 mg/（kg·d）]、高[10.0 mg/（kg·d）]剂量组,分别给予生理盐水和不同剂量的龙胆苦苷处理4周。4周后进行心脏超声检查,并测量心脏重量/体重（HW/BW）、心脏重量/胫骨长度（HW/TL）、左心室舒张期末内径（LVEDD）、左心室收缩期末内径（LVESD）、左心室射血分数（LVEF）和短轴缩短率（FS）。PCR技术检测心肌组织中心房钠尿肽（ANP）、脑钠尿肽（BNP）、β肌球蛋白重链（β-MHC）表达的水平,并行病理学检查。结果与心肌肥厚模型组相比,龙胆苦苷[当剂量达到10.0 mg/（kg·d）]干预4周后,LVEDD较之下降24.9%,LVESD较之下降26.3%;LVEF较之升高49.5%,FS较之升高62.6%,差异均有统计学意义。初步证实龙胆苦苷能够显著降低心肌肥厚参数（心脏重量/体重）（P〈0.01）,显著降低心肌细胞平均横截面积（P〈0.01）。与心肌肥厚模型组相比,龙胆苦苷组ANP、BNP和β-MHC的表达水平显著降低（P〈0.05）。结论龙胆苦苷对压力超负荷等诱导的心肌肥厚有保护作用。

英文摘要：

Aim To investigate the protective effect of pretreatment with Gentiopicroside on transverse aortic constriction（ TAC）-induced myocardial hypertrophy. Methods 40 male C57 BL mice were randomly divided into two groups： sham group（ n = 6） and myocardial hypertrophy model group（ n = 32）. Mice in myocardial hypertrophy group were operated transverse aortic constriction. 24 h later,the mice in myocardial hypertrophy group were randomly divided into 4 groups： myocardial hypertrophy model group,Gentiopicroside high,middle and low dose group,which were given physiological saline and different doses of Gentiopicroside for 4 weeks. Echocardiogram was performed to assess the cardiac function changes. Heart weight to body weight ratio（ HW / BW）,heart weight / tibial length（ HW / TL）,left ventricular end-diastolic diameter（ LVEDD）,left ventricular end-systolic diameter（ LVESD）,left ventricular ejection fraction（ LVEF）and left ventricular fractional shortening（ FS） were measured. The expression levels of atrial natriuretic peptide（ ANP）,brain natriuretic peptide（ BNP）,and β-myosin heavy chain（ β-MHC） in heart tissues and the size of cardiomyocytes were also observed. Results Compared with myocardial hypertrophy model group,the LVEDD decreased 24. 9% in Gentiopicroside group（ especially dose up to 10. 0 mg /（ kg · d）,the LVESD decreased 26. 3%; while the LVEF increased49. 5%,the FS increased 62. 6%,respectively（ P 〈 0. 01）. The HW / BW and the cardiac myocyte cross-sectional area showed a decrease in Gentiopicroside group compared with myocardial hypertrophy model group（ P 〈 0. 01）,while still increased significantly compared with the normal control group. The expression of ANP,BNP and β-MHC in Gentiopicroside group were lower than those in myocardial hypertrophy model group（ P 〈 0. 05）. Conclusion Gentiopicroside can intervene the progress of pressure overload-induced myocardial hypertrophy in C57 BL mice.