ArticleIn vivo (Athens, Greece)
Ferrochel Alleviates Renal Fibrosis by Modulating Fibrogenesis and Epithelial-to-Mesenchymal Transition:
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Abstract
BACKGROUND/
aimFerrochel consists of one ferrous ion chelated with two glycine molecules and is characterized by high bioavailability and physiological activity. However, its potential anti-fibrotic effects and underlying mechanisms remain need clarified. The aim of this study was to determine whether Ferrochel exerts anti-fibrotic activity in renal fibrosis and to clarify the mechanisms by which it may regulate fibrosis and epithelial-mesenchymal transition. MATERIALS AND
methodsA mouse renal tubulointerstitial fibrosis model was established by applying unilateral ureteral obstruction (UUO). Renal morphology, collagen deposition, and iron content were evaluated using hematoxylin and eosin (H&E) staining and Masson's trichrome staining. The expression of fibrosis- and epithelial-mesenchymal transition (EMT)-related proteins was assessed using immunohistochemistry (IHC) and immunoblotting. Cytotoxicity and cell motility were examined using the MTT assay and wound healing assay, respectively.
resultsFerrochel treatment significantly reduced collagen deposition and renal injury in UUO mice without inducing iron accumulation. Moreover, Ferrochel reduced the expression of fibrosis markers (α-SMA and collagen I) and the EMT marker vimentin in the UUO model. In HK2 cells, Ferrochel did not exhibit cytotoxicity. However, it markedly attenuated transforming growth factor-beta1 (TGF-β1)-induced cell motility and decreased the expression of fibrosis markers (α-SMA and collagen I) as well as the EMT marker vimentin in TGF-β1-treated HK2 cells.
conclusionFerrochel attenuated renal fibrogenesis and EMT
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