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标题：Role of Nitric Oxide in Ginsenoside Rg1-Induced Protection against Left Ventricular Hypertrophy Produced by Abdominal Aorta Coarctation in Rats
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作者：Jiang Deng ; Yi-Wei Wang ; Wen-Ming Chen 等
期刊名称：Biological and Pharmaceutical Bulletin
印刷版ISSN：0918-6158
电子版ISSN：1347-5215
出版年度：2010
卷号：33
期号：4
页码：631-635
DOI：10.1248/bpb.33.631
出版社：The Pharmaceutical Society of Japan
摘要：Ginsenoside Rg₁ (Rg₁), one of the active components of Panax ginseng, has been reported to promote endogenous nitric oxide (NO) production in some tissues, and to inhibit left ventricular (LV) hypertrophy in rats. This study aimed to investigate whether Rg₁-induced inhibition of rat LV hypertrophy is mediated by NO-production. Rat LV hypertrophy was induced by abdominal aorta coarctation. Rg₁ 15 mg/kg/d, L -arginine 200 mg/kg/d, and the nitric oxide synthase (NOS) inhibitor N ^G-nitro- L -arginine-methyl ester ( L -NAME) 100 mg/kg/d used with the same dose of L -arginine or Rg₁ were given starting from 1 d after surgery for 21 consecutive days. LV hypertrophy was evidenced by determining LV weight and mRNA expression of atrial natriuretic peptide, a marker of cardiac hypertrophic response, as well as by histopathology. Rg₁ and L -arginine administration significantly reduced the elevated LV hypertrophic parameters independent of LV systolic pressure changing, and ameliorated the histopathology of LV myocardium and LV diastolic function. All the beneficial effects of Rg₁ and L -arginine were abolished or blunted by L -NAME. Further to examine the role of NO in Rg₁ inhibition on LV hypertrophy, expression of endothelial NOS was determined at the transcript levels. In our experimental conditions endothelial NOS mRNA expression in LV tissue was lowered by abdominal aorta coarctation, and upregulated by Rg₁ administration. These results demonstrate that Rg₁-induced protection against LV hypertrophy elicited by abdominal aorta coarctation in rats is mediated, at least in part, via endogenous NO production and release.
关键词：ginsenoside Rg1;left ventricular hypertrophy;endothelial nitric oxide synthase;nitric oxide