Ginsenoside Rg1 Epigenetically Modulates Smad7 Expression in Liver Fibrosis via MicroRNA-152
Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial–mesenchymal transition (EMT) plays a key role in the activation of hepatic stellate cells (HSCs). Recently, Rg1 has been shown to reverse...
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Published in | Journal of ginseng research Vol. 47; no. 4; pp. 534 - 542 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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Korea (South)
Elsevier B.V
01.07.2023
고려인삼학회 Elsevier |
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Abstract | Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial–mesenchymal 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 β (TGF-β) pathway, is often methylated during liver fibrosis. Whether Smad7 methylation plays a vital role in the effects of Rg1 on liver fibrosis remains unclear.
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.
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-β 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.
Rg1 inhibits HSC activation by epigenetically modulating Smad7 expression and at least by partly inhibiting EMT.
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AbstractList | Background: Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial–mesenchymal 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 β (TGF-β) 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-β 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. Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial–mesenchymal 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 β (TGF-β) pathway, is often methylated during liver fibrosis. Whether Smad7 methylation plays a vital role in the effects of Rg1 on liver fibrosis remains unclear. 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. 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-β 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. Rg1 inhibits HSC activation by epigenetically modulating Smad7 expression and at least by partly inhibiting EMT. [Display omitted] BackgroundGinsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial-mesenchymal 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 β (TGF-β) pathway, is often methylated during liver fibrosis. Whether Smad7 methylation plays a vital role in the effects of Rg1 on liver fibrosis remains unclear. MethodsAnti-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. ResultsRg1 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-β 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. ConclusionRg1 inhibits HSC activation by epigenetically modulating Smad7 expression and at least by partly inhibiting EMT. 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 reverseliver fibrosis by suppressing EMT, although the mechanism of Rg1-mediated anti-fibrosis effects is stilllargely 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 theeffects 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 collagendeposition was also observed. Rg1 also contributed to the suppression of collagenation and HSCreproduction 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 Smad7expression and demethylation. The over-expression of DNA methyltransferase 1 (DNMT1) blocked theRg1-mediated inhibition of Smad7 methylation, and miR-152 targeted DNMT1. Further experimentssuggested that Rg1 repressed Smad7 methylation via miR-152-mediated DNMT1 inhibition. MiR-152inhibition 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 bypartly inhibiting EMT. KCI Citation Count: 0 Image 1 Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the epithelial-mesenchymal 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 β (TGF-β) pathway, is often methylated during liver fibrosis. Whether Smad7 methylation plays a vital role in the effects of Rg1 on liver fibrosis remains unclear. Anti-fibrosis effects were examined after Rg1 processing and . Smad7 expression, Smad7 methylation, and microRNA-152 (miR-152) levels were also analyzed. 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-β 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. Rg1 inhibits HSC activation by epigenetically modulating Smad7 expression and at least by partly inhibiting EMT. |
Author | Lang, Zhichao Li, Chunxue Li, Xinmiao Zhan, Yating Zheng, Jianjian Tao, Qiqi Zhang, Rongrong Gao, Yuxiang |
Author_xml | – sequence: 1 givenname: Rongrong surname: Zhang fullname: Zhang, Rongrong – sequence: 2 givenname: Xinmiao surname: Li fullname: Li, Xinmiao – sequence: 3 givenname: Yuxiang surname: Gao fullname: Gao, Yuxiang – sequence: 4 givenname: Qiqi surname: Tao fullname: Tao, Qiqi – sequence: 5 givenname: Zhichao surname: Lang fullname: Lang, Zhichao – sequence: 6 givenname: Yating surname: Zhan fullname: Zhan, Yating – sequence: 7 givenname: Chunxue surname: Li fullname: Li, Chunxue – sequence: 8 givenname: Jianjian orcidid: 0000-0003-0563-2229 surname: Zheng fullname: Zheng, Jianjian email: 120378196@qq.com |
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CitedBy_id | crossref_primary_10_1016_j_heliyon_2024_e29169 crossref_primary_10_1186_s13148_024_01663_5 crossref_primary_10_1016_j_jgr_2024_04_001 crossref_primary_10_1007_s13668_023_00514_8 crossref_primary_10_1039_D3FO03643J crossref_primary_10_1016_j_jpha_2023_11_009 crossref_primary_10_3390_ani13233723 |
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Keywords | Cur DNMT1 PTCH1 MiRNA Ginsenoside Rg1 EMT ECM CCl4-induced fibrosis 5-Aza α-SMA MiR-152 UTR CCl4 Edu TGF-β MiRNAs HSCs MRNA MiR-NC CCl₄-induced fibrosis |
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contributor: fullname: Chang |
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Snippet | Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that the... BackgroundGinsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that... Image 1 Background: Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory, anti-cancer, and hepatoprotective effects. It is known that... Background: Ginsenoside Rg1, a bioactive component of Ginseng, has demonstrated anti-inflammatory,anti-cancer, and hepatoprotective effects. It is known that... |
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StartPage | 534 |
SubjectTerms | CCl4-induced fibrosis Ginsenoside Rg1 MiRNA 기타의약학 |
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Title | Ginsenoside Rg1 Epigenetically Modulates Smad7 Expression in Liver Fibrosis via MicroRNA-152 |
URI | https://dx.doi.org/10.1016/j.jgr.2022.12.005 https://www.dbpia.co.kr/journal/articleDetail?nodeId=NODE11469335 https://www.ncbi.nlm.nih.gov/pubmed/37397418 https://search.proquest.com/docview/2832843479 https://pubmed.ncbi.nlm.nih.gov/PMC10310870 https://doaj.org/article/2c10988ecc9b483d9fcdee4ef1506e09 https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART003016124 |
Volume | 47 |
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ispartofPNX | Journal of Ginseng Research, 2023, 47(4), , pp.534-542 |
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