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目的:研究人参皂苷Rg1(ginsenoside Rg1)对主动脉缩窄致左室肥厚大鼠模型的保护作用,并对其作用机制作初步探讨.方法:通过结扎成年雄性大鼠胸主动脉法构建大鼠心肌肥厚模型,将胸主动脉缩窄造模成功的24只SD大鼠随机分为单纯手术组(TAC组)及Rg1治疗组(Rg1组).另外,将假结扎胸主动脉的12只大鼠作为假手术组(Sham组).4周后分离左室称重,测定各组大鼠左心室质量指数(left ventricular mass index,LVMI);采用HE染色观察心室壁厚度、心肌组织结构;采用Real-time PCR法检测左室心肌组织中心房利钠因子(ANF)、B型脑利钠肽(BNP)和缺氧诱导因子1α(hypoxia inducible factor-1α,HIF-1α)的mRNA表达;采用Western blot法检测左室心肌组织中HIF-1α蛋白表达.结果:与TAC组相比,人参皂苷Rg1给药组动物的左心室质量指数、心肌细胞肥大程度、ANP、BNP表达均有显著下降(P<0.05);HIF-1α的mRNA和蛋白的表达均有显著增加(P<0.05).结论:人参皂苷Rg1有效地缓解压力超负荷诱导的大鼠心肌肥厚并改善左室功能,而这种保护作用可能通过增加HIF-1α表达有关.“,”Objective:To investigate the beneficial effects of ginsenoside Rg1(Rg1) in the treatment of cardiac hypertrophy induced by transverse aortic contraction(TAC) and the potential molecular mechanisms in rats.Methods:Adult male SD rats were conducted in the study;twenty-four rats which are managed to present left ventricular hypertrophy(LVH) after TAC were randomly divided into two groups:the TAC group and the Rg1 group.Another 12 rats which was absence of the aortic artery ligated after analogous operation was included in the Sham group.The administration of Rg1 was conducted at 10 mg/(kg.d) for 4 weeks.After that,the left ventricular mass index(LVMI) were examined as hypertrophic parameters;left ventricle sections were stained with hematoxylin and eosin for ventricular wall thickness and myocardial microstructure.The mRNA transcription of ANP,BNP and HIF1α was detected by Real-time quantitative PCR.The protein expression of HIF-1α was evaluated through Western blot test.Results: Compared with TAC group,the treatment with Rg1 significantly reduced the LVMI,the size of cardiomyocyte,and the mRNA expression of transcripts of ANF,BNP(P<0.05,respectively).In the Rg1 group,the protein and mRNA levels of HIF-1α were significantly increased comparing to the control group(P<0.05,respectively).Conclusion:Ginsenoside Rg1 attenuates the left ventricular hypertrophy and improves the cardiac function in the experimental rat model after TAC undertaken.This beneficial effects may be partially attributed to the increase of HIF-1α expression.