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Red ginseng extract protects against carbon tetrachloride-induced liver fibrosis
Korean red ginseng, the processed root of Panax ginseng Meyer, has been frequently used for various therapeutic purposes in oriental medicine. The present study investigated the possible effect of Korean red ginseng extract (RGE) for the treatment of liver fibrosis in mice injected with carbon tetra...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Ginseng
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3659625/ https://www.ncbi.nlm.nih.gov/pubmed/23717156 http://dx.doi.org/10.5142/jgr.2013.37.45 |
Sumario: | Korean red ginseng, the processed root of Panax ginseng Meyer, has been frequently used for various therapeutic purposes in oriental medicine. The present study investigated the possible effect of Korean red ginseng extract (RGE) for the treatment of liver fibrosis in mice injected with carbon tetrachloride (CCl(4)) for 4 wk. Liver injuries were assessed by blood biochemistry and histopathology in mice treated with CCl(4) alone or CCl(4)+ RGE (30, 100, and 300 mg/kg). Concomitant treatment with RGE and CCl(4) (three times/wk for 4 wk) effectively inhibited liver fibrosis as evidenced by decreases in plasma alanine and aspartate aminotransferases, as well as by the percentages of degenerative regions, numbers of degenerative hepatocytes, and collagen accumulation in hepatic parenchyma. Treatment with CCl(4) for 4 wk increased mRNA levels of transforming growth factor β1 and plasminogen activator inhibitor 1 in fibrogenic liver, whereas RGE (30, 100, and 300 mg/kg) significantly blocked the induction of fibrogenic genes by CCl(4). Similarly, RGE also prevented transforming growth factor β1-mediated induction of fibrogenic genes in human hepatic stellate cell lines. More importantly, RGE markedly reduced the number of α-smooth muscle actin-positive cells in liver tissue. This study implies that RGE efficaciously protects against the liver fibrosis induced by chronic CCl(4) treatment, and may therefore have potential to treat liver disease. |
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