The role of pirfenidone in alkali burn rat cornea

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Abstract

To evaluate the effects of pirfenidone in the treatment of HUVEC using an in vitro model and on rat corneal wound healing, edema, cornea neovascularization (CNV) and inflammation after alkali burn in vivo model. In vitro, CCK-8 assay was used to detect the effect of pirfenidone on the viability of HUVECs. The effects of pirfenidone on migration and tube formation of HUVEC were evaluated by HUVEC cell wound closure and tube formation assay. In vivo, Eye drops containing pirfenidone or phosphate buffered saline (PBS) were administered to an alkali-burn-induced corneal inflammatory and neovascularization model four times daily. The clinical evaluations, including fluorescent staining and cornea edema, were performed on days 1, 4, 7 and 14 using slit lamp microscopy. Global specimens were collected on day 7 and processed for immunofluorescent staining Collagen IV, α-smooth muscle actin (α-SMA), vascular endothelial growth factor (VEGF), pigment epithelium derived factor (PEDF) and cluster of differentiation34 (CD34). The levels of α-SMA, VEGF, PEDF, CD34, CD31 and nuclear factor-kappa B (NF-κB) proteins in the corneas were determined by western blot. Pirfenidone affects HUVEC viability, migration and tube formation in a dose-dependent manner. High concentration of pirfenidone can inhibit HUVEC viability, migration and tube formation in vitro and reduce alkali burn rat cornea edema, promote corneal wound healing, inhibit CNV and inflammation after alkali burn in vivo. Pirfenidone promotes corneal wound healing, and inhibits cornea neovascularization and inflammation after alkali burn in vitro and in vivo. Pirfenidone may be the potential anti-inflammation agent for the clinical treatment of CNV.

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