Tropical Journal of Pharmaceutical Research

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Hepatoprotective effects of ginseng saponins in a mouse model of carbon tetrachloride-induced liver injury

Huizhi Lu, Yun Tan Tan, Luyu Yang, Hui Dong, Youxia Liao, Song Cao, Shouzhi Fu


Purpose: To investigate the effects of ginsenosides Rg1 and Rb1 on carbon tetrachloride (CCl4)-induced liver injury in mice.

Methods: Thirty-two mice were randomly divided into four groups. In control group, mice were administered sodium carboxymethylcellulose (CMC-Na) by intraperitoneal injection for seven days. In CCl4 treatment group, mice were treated as control group for the first seven days and then intraperitoneally injected with CCl4 in olive oil on day 8. In Rb1- and Rg1-treatment group, the mice were intraperitoneally injected with Rb1 or Rg1 (each 30 mg/kg, dissolved in 0.5 % CMC-Na), respectively for seven days, followed by intraperitoneal injection with CCl4 in olive oil on day 8. Histological damage was examined by haematoxylin and eosin (H&E) staining. Serum levels of alanine aminotransferase (ALT) and aspartate transaminase (AST) were assessed enzymatically. Tissue IL-6 and IL-8 levels were measured by ELISA. Gene and protein levels of transforming growth factor (TGF)-β, Smad2, and Smad3 were analyzed by real-time PCR (RT-PCR) and western blotting, respectively.

Results: CCl4 treatment caused histological damage in mouse liver, and increased the levels of ALT, AST (five-fold), IL-6 (three-fold), and IL-8 (five-fold), and elevated expressions of TGF-β, Smad2, and Smad3. Ginsenosides Rg1 or Rb1 pre-treatment attenuated liver injury by decreasing the serum levels of ALT (from 700 to 200 UI/L) AST (from 550 pg/mL to 250 pg/ml), IL-6 (from 1,100 to 750 pg/mL), and IL-8 (from 600 to 200 pg/mL), and inhibiting the expressions of TGF-β, Smad2, and Smad3.

Conclusion: Ginsenosides (Rg1 and Rb1) attenuate CCl4-induced liver injury and inflammation by regulating TGF-β/Smad signalling pathway.

Keywords: Ginseng saponin, Ginsenosides, Rg1, Rb1, Hepatoprotective effect, TGF-β/Smad signalling pathway
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