In vivo (Athens, Greece) · 2026
Ferrochel Alleviates Renal Fibrosis by Modulating Fibrogenesis and Epithelial-to-Mesenchymal Transition: In Vitro and In Vivo Studies.
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Lee Chien-Hsing, Chen Wei-Liang, Lin Wen-Hua, Ting Yi-Hsuan, Hung Tung-Wei, Hsieh Yi-Hsien
Аннотация
BACKGROUND/AIM: Ferrochel 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 METHODS: A 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.
RESULTS: Ferrochel 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.
CONCLUSION: Ferrochel attenuated renal fibrogenesis and EMT in vitro and in vivo, indicating anti-fibrotic activity. These results suggest that Ferrochel may serve as a potential therapeutic agent for renal tubulointerstitial fibrosis.
MATERIALS AND METHODS: A 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.
RESULTS: Ferrochel 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.
CONCLUSION: Ferrochel attenuated renal fibrogenesis and EMT in vitro and in vivo, indicating anti-fibrotic activity. These results suggest that Ferrochel may serve as a potential therapeutic agent for renal tubulointerstitial fibrosis.