上皮-间质转换
体内
化学
活性氧
纤维化
SMAD公司
转化生长因子
人参皂苷Rg1
癌症研究
细胞凋亡
药理学
间充质干细胞
人参皂甙
人参
内科学
医学
生物化学
病理
生物
下调和上调
替代医学
生物技术
基因
作者
Xiaoyü Wei,Yatang Chen,Wenxiang Huang
出处
期刊:Biofactors
[Wiley]
日期:2018-05-15
卷期号:44 (4): 327-335
被引量:26
摘要
Liver fibrosis remains a major cause of morbidity and mortality with a complicated etiology and notorious complications, but there is a lack of efficacious therapeutics. Epithelial to mesenchymal transition (EMT) has a central role in the course of liver fibrosis, and thus, prevention of the development of EMT may control and even reverse liver fibrosis. This study aimed to examine the beneficial effect of ginsenoside Rg1, a phrenological active component isolated from Ginseng, and interrogate the mechanism in vitro and in vivo, with a focus on transforming growth factor-β (TGF-β)/Smad and Nrf2-mediated signaling pathways. We employed a TGF-β-induced EMT model in HSC-T6 cells and CCl4 -induced liver fibrosis in animal. We found that ginsenoside Rg1 significantly reduced cell proliferation and reversed transforming growth factor-β (TGF-β)-induced EMT in HSC-T6 cells; and ginsenoside Rg1 induced cell apoptosis, Ginsenoside Rg1 decreased the cellular level of collagen I and III in HSC-T6 cells, indicating the amelioration of fibrosis. We showed that ginsenoside Rg1 reduced cellular reactive oxygen species (ROS). We also observed similar beneficial effects of ginsenoside Rg1 in vivo. The data showed that ginsenoside Rg1 decreased the level of alanine aminotransferase and aspartate aminotransferase, and collage type IV (IV-C), hyaluronic acid, and laminin in carbon tetrachloride (CCl4)-induced liver fibrotic model. Mechanistically, we showed that ginsenoside Rg1 tuned down the TGF-β/Smad and stimulated Nrf-2 nuclear translocation, which could explain the beneficial effects. In aggregate, our results demonstrate that ginsenoside Rg1 exhibits a protective effect on liver fibrosis via suppressing EMT and cellular ROS level. © 2018 BioFactors, 2018.
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