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Ginsenoside Rb1 Attenuates TGF-β1-Induced MUC4/5AC Expression and Epithelial-Mesenchymal Transition in Human Airway Epithelial Cells / 대한이비인후과학회지
Korean Journal of Otolaryngology - Head and Neck Surgery ; : 232-239, 2021.
Article in Korean | WPRIM | ID: wpr-920145
ABSTRACT
Background and Objectives@#Ginsenoside Rb1 is the main metabolite of Panax ginseng. It is known to have many beneficial properties including anti-inflammatory, antitumoral and antioxidant effects. However, the therapeutic effects of ginenoside Rb1 on inflammatory airway diseases have not been elucidated. Therefore, we investigated the effects of ginsenoside Rb1 on the TGF-β1-induced mucin gene expression and epithelial-mesenchymal transition (EMT) in human airway epithelial cells.Materials and Method We evaluated the effects of ginsenoside Rb1 on the changes of MUC4, MUC5AC, occludin, claudin 4, claudin 18, neural (N)-cadherin, and epithelial (E)-cadherin expression by TGF-β1 in NCI-H292 cells using reverse, real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and western blot. @*Results@#TGF-β1 significantly increased MUC4/5AC expression. Rb1 inhibited TGF-β1- induced MUC4/5AC expression. In addition, TGF-β1 significantly attenuated occludin, claudin 18, and E-cadherin expressions but induced claudin 4 and N-cadherin expressions. On the other hand, Rb1 reversed changes in the TGF-β1- mediated expressions of cell junction molecules. @*Conclusion@#These results suggest that ginsenoside Rb1 attenuates TGF-β1-induced MUC4/5AC expressions and EMT in the human airway epithelial cells. These findings are important data demonstrating the potential of ginsenoside Rb1 as a therapeutic agent for inflammatory airway diseases.
Full text: Available Index: WPRIM (Western Pacific) Language: Korean Journal: Korean Journal of Otolaryngology - Head and Neck Surgery Year: 2021 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Korean Journal: Korean Journal of Otolaryngology - Head and Neck Surgery Year: 2021 Type: Article