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dc.contributor.authorRattiyaporn Kanlayaen_US
dc.contributor.authorPaleerath Peerapenen_US
dc.contributor.authorAngkhana Nilnumkhumen_US
dc.contributor.authorSirikanya Plumworasawaten_US
dc.contributor.authorKanyarat Sueksakiten_US
dc.contributor.authorVisith Thongboonkerden_US
dc.contributor.otherFaculty of Medicine, Siriraj Hospital, Mahidol Universityen_US
dc.date.accessioned2020-01-27T03:29:25Z-
dc.date.available2020-01-27T03:29:25Z-
dc.date.issued2020-02-01en_US
dc.identifier.citationJournal of Nutritional Biochemistry. Vol.76, (2020)en_US
dc.identifier.issn18734847en_US
dc.identifier.issn09552863en_US
dc.identifier.other2-s2.0-85075265771en_US
dc.identifier.urihttp://repository.li.mahidol.ac.th/dspace/handle/123456789/49536-
dc.description.abstract© 2019 Several lines of evidence have demonstrated anti-fibrotic property of epigallocatechin-3-gallate (EGCG) in many tissues/organs but with unclear mechanisms. This study thus aimed to define cellular mechanisms underlying such protective effect of EGCG. HK-2 renal cells were treated with 5 ng/ml TGF-β1 for 24 h with/without pretreatment by 5 μM EGCG for 1 h. The cells were then evaluated by morphological examination, immunofluorescence study, semi-quantitative RT-PCR, Western blotting, and atomic force microscopy (AFM). The results showed that TGF-β1-treated cells underwent epithelial mesenchymal transition (EMT) as evidenced by morphological change into fibroblast-like and increases in spindle index, mesenchymal markers (Snail1 and vimentin), extracellular matrix (fibronectin), cell stiffness (by AFM measurement) and actin stress fibers, whereas the epithelial markers (E-cadherin and ZO-1) were decreased. All of these features were abolished by EGCG pretreatment. Functional studies revealed that the anti-fibrotic property of EGCG was, at least in part, due to de-activation/stabilization of GSK-3β/β-catenin/Snail1 (EMT-triggering) signaling pathway that was activated by TGF-β1 as shown by maintaining phosphorylated GSK-3β, β-catenin and Snail1 to their basal levels. Additionally, Nrf2 knockdown by small interfering RNA could abolish the EGCG effect on β-catenin expression. These data indicate that EGCG attenuates TGF-β1-induced EMT in renal tubular cells through GSK-3β/β-catenin/Snail1 and Nrf2 pathways.en_US
dc.rightsMahidol Universityen_US
dc.source.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85075265771&origin=inwarden_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectMedicineen_US
dc.subjectNursingen_US
dc.titleEpigallocatechin-3-gallate prevents TGF-β1-induced epithelial-mesenchymal transition and fibrotic changes of renal cells via GSK-3β/β-catenin/Snail1 and Nrf2 pathwaysen_US
dc.typeArticleen_US
dc.rights.holderSCOPUSen_US
dc.identifier.doi10.1016/j.jnutbio.2019.108266en_US
dc.identifier.urlhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85075265771&origin=inwarden_US
Appears in Collections:Scopus 2020

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