Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40290
DC FieldValueLanguage
dc.contributor.authorChiang, C.K.en_US
dc.contributor.author許美鈴zh_TW
dc.contributor.authorSheu, M.L.en_US
dc.contributor.authorLin, Y.W.en_US
dc.contributor.authorWu, C.T.en_US
dc.contributor.authorYang, C.C.en_US
dc.contributor.authorChen, M.W.en_US
dc.contributor.authorHung, K.Y.en_US
dc.contributor.authorWu, K.D.en_US
dc.contributor.authorLiu, S.H.en_US
dc.date2011zh_TW
dc.date.accessioned2014-06-06T08:03:33Z-
dc.date.available2014-06-06T08:03:33Z-
dc.identifier.issn0007-1188zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/40290-
dc.description.abstractBACKGROUND AND PURPOSE Renal fibrosis acts as the common pathway leading to the development of end-stage renal disease. The present study investigated, in vivo and in vitro, the anti-fibrotic and anti-inflammatory effects, particularly on the epithelial to mesenchymal transition of renal tubular cells, exerted by honokiol, a phytochemical used in traditional medicine, and mechanisms underlying these effects. EXPERIMENTAL APPROACH Anti-fibrotic effects in vivo were assayed in a rat model of renal fibrosis [the unilateral ureteral obstruction (UUO) model]. A rat tubular epithelial cell line (NRK-52E) was stimulated by transforming growth factor-beta 1 (TGF-beta 1) and treated with honokiol to explore possible mechanisms of these anti-fibrotic effects. Gene or protein expression was analysed by Northern or Western blotting. Transcriptional regulation was investigated using luciferase activity driven by a connective tissue growth factor (CTGF) promoter. KEY RESULTS Honokiol slowed development of renal fibrosis both in vivo and in vitro. Honokiol treatment attenuated tubulointerstitial fibrosis and expression of pro-fibrotic factors in the UUO model. Honokiol also decreased expression of the mRNA for the chemokine CCL2 and for the intracellular adhesion molecule-1, as well as accumulation of type I (alpha 1) collagen and fibronectin in UUO kidneys. Phosphorylation of Smad-2/3 induced by TGF-beta 1 and CTGF luciferase activity in renal tubular cells were also inhibited by honokiol. CONCLUSIONS AND IMPLICATIONS Honokiol suppressed expression of pro-fibrotic and pro-inflammatory factors and of extracellular matrix proteins. Honokiol may become a therapeutic agent to prevent renal fibrosis.en_US
dc.language.isoen_USzh_TW
dc.relationBritish Journal of Pharmacologyen_US
dc.relation.ispartofseriesBritish Journal of Pharmacology, Volume 163, Issue 3, Page(s) 586-597.en_US
dc.relation.urihttp://dx.doi.org/10.1111/j.1476-5381.2011.01242.xen_US
dc.titleHonokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro-inflammatory factors in vivo and in vitroen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1111/j.1476-5381.2011.01242.xzh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.fulltextno fulltext-
item.languageiso639-1en_US-
item.grantfulltextnone-
Appears in Collections:生物醫學研究所
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