title: Ginsenoside Rb1 inhibits cell activation and liver fibrosis in rat hepatic stellate cells.
abstract: Chronic hepatitis/cirrhosis is the eighth leading cause of death in Taiwan. Excess accumulated extracellular matrix produced by activated hepatic stellate cells (HSCs) is the major cause of liver fibrosis. Ginsenoside Rb1, the most active compound purified from ginseng, has been considered to be hepatoprotective. This study investigated the effects of ginsenoside Rb1 (98.8% purity) on activation, proliferation, and profibrotic factors in rat HSC-T6 cells under H₂O₂ oxidative stress. Rat HSC-T6 cells were activated by 10 nM H₂O₂ and then incubated with different concentrations of ginsenoside Rb1 (5, 10, 20, 40, and 80 μg/mL) for 24 hours. Medium containing 0.08% dimethyl sulfoxide or 5 mM N-acetyl-l-cysteine was used as a negative or positive control, respectively. The results showed that ginsenoside Rb1 at 5-40 μg/mL significantly reduced α-smooth muscle actin levels and at 5-80 μg/mL inhibited cell proliferation in HSC-T6 cells after induction with H₂O₂ (P<.05). Collagen secreted by HSC-T6 cells was decreased by ginsenoside Rb1 at 5-80 μg/mL (P<.05). Protein expression of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase (MMP)-2, and tissue inhibitor of metalloproteinase (TIMP)-1 was suppressed by ginsenoside Rb1 at 10-80 μg/mL (P<.05). In addition, mRNA expression of type I and III collagen, TGF-β1, and TIMP-1 was inhibited by ginsenoside Rb1 (10 and 80 μg/mL) (P<.05). Therefore, ginsenoside Rb1 exerted an antifibrotic effect on HSCs by inhibiting activation, proliferation, and expression of collagen, TGF-β1, MMP-2, and TIMP-1.
authors: School of Nutrition and Health Sciences, Taipei Medical University, Taipei, Taiwan.
authors: Yu-Ting
authors: YT
authors: Lo
authors: Ya-Hui
authors: YH
authors: Tsai
authors: Shu-Ju
authors: SJ
authors: Wu
authors: Jiun-Rong
authors: JR
authors: Chen
authors: Jane C-J
authors: JC
authors: Chao
mesh_terms: D000111:Acetylcysteine / Q000378:metabolism; D000818:Animals; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival; D003094:Collagen / Q000378:metabolism; D004121:Dimethyl Sulfoxide / Q000378:metabolism; D036145:Ginsenosides / Q000494:pharmacology*; D055166:Hepatic Stellate Cells / Q000166:cytology* / Q000187:drug effects*; D006861:Hydrogen Peroxide / Q000378:metabolism; D008103:Liver Cirrhosis / Q000188:drug therapy / Q000473:pathology; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D013624:Taiwan; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000235:genetics / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism
chemical_list: D036145:Ginsenosides; D019715:Tissue Inhibitor of Metalloproteinase-1; D053773:Transforming Growth Factor beta1; C442759:ginsenoside Rb1; D003094:Collagen; D006861:Hydrogen Peroxide; D020778:Matrix Metalloproteinase 2; C522363:Mmp2 protein, rat; D000111:Acetylcysteine; D004121:Dimethyl Sulfoxide