Ginsenoside Rg1 Epigenetically Modulates Smad7 Expression in Liver Fibrosis via MicroRNA-152

Rongrong Zhang; Xinmiao Li; Yuxiang Gao; Qiqi Tao; Zhichao Lang; Yating Zhan; Chunxue Li; Jianjian Zheng

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자료유형: 학술저널

저자정보: Rongrong Zhang (The First Affiliated Hospital of Wenzhou Medical University) Xinmiao Li (The First Affiliated Hospital of Wenzhou Medical University) Yuxiang Gao (The First Affiliated Hospital of Wenzhou Medical University) Qiqi Tao (The First Affiliated Hospital of Wenzhou Medical University) Zhichao Lang (The First Affiliated Hospital of Wenzhou Medical University) Yating Zhan (The First Affiliated Hospital of Wenzhou Medical University) Chunxue Li (The First Affiliated Hospital of Wenzhou Medical University) Jianjian Zheng (The First Affiliated Hospital of Wenzhou Medical University)

저널정보: 고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.47 No.4

발행연도: 2023.7

수록면: 534 - 542 (9page)

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Background: Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelialemesenchymal transition (EMT) plays a key role in the activation of hepatic stellate cells (HSCs). Recently, Rg1 has been shown to reverse liver fibrosis by suppressing EMT, although the mechanism of Rg1-mediated anti-fibrosis effects is still largely unclear. Interestingly, Smad7, a negative regulator of the transforming growth factor b (TGF-b) pathway, is often methylated during liver fibrosis. Whether Smad7 methylation plays a vital role in the effects of Rg1 on liver fibrosis remains unclear.
Methods: Anti-fibrosis effects were examined after Rg1 processing in vivo and in vitro. Smad7 expression, Smad7 methylation, and microRNA-152 (miR-152) levels were also analyzed.
Results: Rg1 significantly reduced the liver fibrosis caused by carbon tetrachloride, and reduced collagen deposition was also observed. Rg1 also contributed to the suppression of collagenation and HSC reproduction in vitro. Rg1 caused EMT inactivation, reducing Desmin and increasing E-cadherin levels. Notably, the effect of Rg1 on HSC activation was mediated by the TGF-b pathway. Rg1 induced Smad7 expression and demethylation. The over-expression of DNA methyltransferase 1 (DNMT1) blocked the Rg1-mediated inhibition of Smad7 methylation, and miR-152 targeted DNMT1. Further experiments suggested that Rg1 repressed Smad7 methylation via miR-152-mediated DNMT1 inhibition. MiR-152 inhibition reversed the Rg1-induced promotion of Smad7 expression and demethylation. In addition, miR-152 silencing led to the inhibition of the Rg1-induced EMT inactivation.
Conclusion: Rg1 inhibits HSC activation by epigenetically modulating Smad7 expression and at least by partly inhibiting EMT.

#CCl₄-induced fibrosis #Ginsenoside Rg1 #MiRNA

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