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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/23612


    Title: In Vitro and In Vivo Antifibrotic Effects of Fraxetin on Renal Interstitial Fibrosis via the ERK Signaling Pathway
    Authors: Hsieh, YH;Hung, TW;Chen, YS;Huang, YN;Chiou, HL;Lee, CC;Tsai, JP
    Keywords: chronic kidney disease;fraxetin;indoxyl sulfate;alpha-SMA;ERK
    Date: 2021
    Issue Date: 2022-08-05T09:40:06Z (UTC)
    Publisher: MDPI
    Abstract: Fraxetin, a natural derivative of coumarin, is known to have anti-inflammatory, anti-oxidant, and hepatoprotective effects in multiple diseases and in liver fibrosis. Whether fraxetin exerts similar effects against renal fibrosis is unknown. In a Unilateral Ureteral Obstruction (UUO) mouse model of renal fibrosis, fraxetin decreased UUO-induced renal dysfunction with a marked reduction in renal interstitial collagen fibers as detected by Masson's Trichrome staining. Fraxetin treatment also inhibited the expression of alpha-SMA, Collagen I, Collagen IV, fibronectin, N-cadherin, vimentin, phosphorylated-ERK, and increased the expression of E-cadherin in UUO mice, as shown by immunohistochemical staining and western blot analysis. In vitro studies showed that fraxetin and indoxyl sulfate had no cytotoxic effects on MES13 kidney cells, but that fraxetin significantly decreased IS-induced cell motility and decreased protein expression of alpha-SMA, N-cadherin, vimentin, and Collagen IV via the ERK-mediated signaling pathway. These findings provide insight into the mechanism underlying fraxetin-induced inhibition of fibrogenesis in renal tissue and suggest that fraxetin treatment may be beneficial for slowing CKD progression.
    URI: http://dx.doi.org/10.3390/toxins13070474
    https://www.webofscience.com/wos/woscc/full-record/WOS:000676943000001
    https://ir.csmu.edu.tw:8080/handle/310902500/23612
    Relation: TOXINS ,2021,v13,issue 7
    Appears in Collections:[中山醫學大學研究成果] 期刊論文

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