Abstract Title:

Ginsenoside-Rg1 from Panax notoginseng prevents hepatic fibrosis induced by thioacetamide in rats.

Abstract Source:

J Zhejiang Univ Sci B. 2006 Aug;7(8):608-14. PMID: 20184879

Abstract Author(s):

JiaWei Geng, Wei Peng, YouGuang Huang, Hong Fan, ShuDe Li

Article Affiliation:

Department of Digestive Diseases, The First People's Hospital of Yunnan Province, Kunming, Yunnan 650032, China.


Panax notoginseng saponins have recently been reported to suppress liver fibrosis. Since ginsenoside-Rg1 is the most abundant component of Panax notoginseng saponins, we investigated the effect of ginsenoside-Rg1 on experimental liver fibrosis in rats. Histological analysis revealed that ginsenoside-Rg1 significantly improved the extent of liver fibrosis in rats induced by thioacetamide. Ginsenoside-Rg1 markedly suppressed the serum levels of fibrotic markers and hepatic hydroxyproline content in rats treated with thioacetamide. Ginsenoside-Rg1 also reduced the serum levels of alanine transaminase, aspartate transaminase and alkaline phosphatase. Finally, ginsenoside-Rg1 attenuated the levels of thiobarbituric acid reactive substances in livers of rats treated by thioacetamide. In cultured hepatic stellate cells, ginsenoside-Rg1 markedly inhibited cell proliferation, activation and formation of reactive oxygen species stimulated by platelet-derived growth factor-BB (PDGF-BB). Additionally, ginsenoside-Rg1 down-regulated the expression of PDGF receptor-beta by reducing the nuclear factor-kappaB activity, which was required for the gene expression. These results suggest that ginsenoside-Rg1, which exhibits its antioxidant and antifibrotic properties, may be of potential therapeutic value in protecting the liver fibrosis.

Study Type : Animal Study

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