Abstract
BackgroundGinsenosides, 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.MethodsMale 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.ResultsThe pathological results showed that ginsenoside Rb1 decreased hepatic fat deposition (2.65 ± 0.82 vs 3.50 ± 0.75, p <0.05) and Panax ginseng extract lowered hepatic reticular fiber accumulation (1.05 ± 0.44 vs 1.60 ± 0.39, p <0.01) increased by CCl4. Plasma alanine aminotransferase and aspartate aminotransferase activities were increased by CCl4 (p <0.01), and aspartate aminotransferase activity was decreased by Panax ginseng extract at week 9 (p <0.05). Exposure to CCl4 for 7 weeks, the levels of plasma and hepatic triglycerides (p <0.01), hepatic cholesterol (p <0.01), interleukin-1β (p <0.01), prostaglandin E2 (p <0.05), soluble intercellular adhesion molecule-1 (p <0.05), hydroxyproline (p <0.05), matrix metalloproteinase-2 (p <0.05) and tissue inhibitor of metalloproteinase-1 (TIMP-1) (p <0.01) were elevated, however, hepatic interleukin-10 level was lowered (p <0.05). Both 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 <0.05).ConclusionsPanax 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.
Highlights
Ginsenosides, the major bioactive compounds in ginseng root, have been found to have antioxidant, immunomodulatory and anti-inflammatory activities
The previous study revealed that ginseng extract rich in ginsenosides suppressed hepatic cholesterol synthesis via inhibiting hepatic β-hydroxy-β-methylglutaryl-CoA reductase and cholesterol 7α-hydroxylase activities [33]. These results suggest that ginseng extract, ginsenoside Rb1 and their metabolite may accelerate lipid utilization and suppress lipid biosynthesis in the liver to further decrease elevated hepatic triglycerides induced by Carbon tetrachloride (CCl4) exposure
Our present study found that ginseng extract and ginsenoside Rb1 significantly decreased hepatic prostaglandin E2 (PGE2) level induced by CCl4
Summary
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. Carbon tetrachloride (CCl4) is considered as a toxic chemical that induces hepatotoxicity including fatty degeneration, inflammation, fibrosis, hepatocellular death and carcinogenicity [5,6]. The toxic metabolite of CCl4 can activate Kupffer cells to secrete cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α), stimulate transforming growth factor-β (TGF-β) production, inhibit nitric oxide (NO) formation and induce inflammation and liver fibrosis [6,7,8]. Chronic exposure of CCl4 leads to liver fibrosis, which diminishes extracellular matrix degradation and increases MMP-2 secretion through the induction of tissue inhibitor TIMPs [9]
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