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Protective effects of total saponins of panax notoginseng on myocardial hypertrophy and fibrosis induced by isoproterenol in rats / 中国病理生理杂志
Article de Zh | WPRIM | ID: wpr-529785
Bibliothèque responsable: WPRO
ABSTRACT
AIM:To investigate the protective effects of total saponins of panax notoginseng (PNS) on myocardial hypertrophy and fibrosis induced by isoproterenol (ISO) in rats. METHODS: Myocardial hypertrophy and fibrosis model of rats were induced by injection of ISO (5 mg?kg-1?d-1, sc) for 7 days. From day 2, the rats were administered with PNS at dose of 25 and 50 mg?kg-1?d-1, ip for 14 days, the control and ISO model group were received saline injection. Then, the heart-weight (HW), left ventricular weight (LVW), the ratio of HW/BW and LVW/BW (LVI) were measured; the hydroxyproline and malondialdehyde (MDA) and angiotensin (AngII) content of left ventricle. The level of nitric oxide (NO), nitric oxide synthase (NOS), superoxide disrnutase (SOD) and glutathione peroxidase (GSH-Px) activities in left ventricle were determined by spectrophotemetry and radioimmunoassay, respectively. RESULTS: Compared with NS control group, the ratio of HW/BW, LVW/BW and the content of hydroxyproline, AngII, MDA and iNOS activity in the left ventricle were significantly increased. The cNOS, SOD, GSH-Px activities and NO content were obriously decreased in the ISO model group. After treatment with PNS, the left ventricular NO content, cNOS, SOD and GSH-Px activities were markedly higher than those in ISO model group. The content of MDA, AngII and iNOS activities and the ratio of HW/BW, LVI were significantly lower than those in ISO model group. CONCLUSION: PNS reverses the myocardial hypertrophy and fibrosis induced by isoproterenol in rats. This effect may be related to eliminating the oxygen free radicals and raising NO level.
Mots clés
Texte intégral: 1 Indice: WPRIM langue: Zh Texte intégral: Chinese Journal of Pathophysiology Année: 2000 Type: Article
Texte intégral: 1 Indice: WPRIM langue: Zh Texte intégral: Chinese Journal of Pathophysiology Année: 2000 Type: Article