Ginseng extract and ginsenoside Rb1 attenuate carbon tetrachloride-induced liver fibrosis in rats

摘要

Background Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities. This study investigated the effects of ginsenosides on carbon tetrachloride (CCl₄)-induced hepatitis and liver fibrosis in rats. Methods Male Sprague–Dawley rats were randomly divided into four groups: control, CCl₄, CCl₄?+?0.5?g/kg Panax ginseng extract and CCl₄?+?0.05?g/kg ginsenoside Rb1 groups. The treated groups were orally given Panax ginseng extract or ginsenoside Rb1 two weeks before the induction of liver injury for successive 9?weeks. Liver injury was induced by intraperitoneally injected with 400?ml/l CCl₄ at a dose of 0.75?ml/kg body weight weekly for 7?weeks. The control group was intraperitoneally injected with olive oil. Results The pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65?±?0.82 vs 3.50?±?0.75, p Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05?±?0.44 vs 1.60?±?0.39, p 4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl₄ (p , and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p 4 for 7?weeks, the levels of plasma and hepatic triglycerides (p p p 2 (p p p p p p Panax ginseng extract and ginsenoside Rb1 decreased plasma and hepatic triglyceride, hepatic prostaglandin E₂, hydroxyproline and TIMP-1 levels, and Panax ginseng extract further inhibited interleukin-1β concentrations (p Conclusions Panax ginseng extract and ginsenoside Rb1 attenuate plasma aminotransferase activities and liver inflammation to inhibit CCl₄-induced liver fibrosis through down-regulation of hepatic prostaglandin E₂ and TIMP-1.