Astragaloside IV inhibits the proliferation and migration of lens epithelial cells induced by TGF-β through the Jagged-1/Notch pathway

Abstract

Aberrant proliferation and migration of residual lens epithelial cells (LECs) is the main cause of posterior capsule opacification (PCO) after cataract surgery. The purpose of this study was to confirm the protective effects of Astragaloside IV (AST) in transforming growth factor beta (TGF-β)-induced proliferation and migration of LECs. Human LECs, SRA01/04, were used in this study. MTT assay and EdU assay were used to perform cell viability and proliferation, respectively. The cell cycle was determined using flow cytometry. Cell invasion and migration were determined using transwell assay and wound healing assay, respectively. Protein expression was examined using western blotting. Type I and IV collagen (Col I and IV) and fibronectin (FN) in cells were also detected using immunofluorescence (IF). Cell viability, proliferation, migration and invasion were suppressed by AST in a concentration-dependent manner in TGF-β-treated LECs. AST stopped the cell cycle at G2 phase in a concentration-dependent manner. Expression of Cyclin B1 and CDK1 was suppressed by AST in TGF-β-treated LECs. Protein expression of FN, Col I, Col IV, α-SMA (α-smooth muscle actin), Snail and Slug was downregulated by AST in a concentration-dependent manner. AST inhibited the protein expression of Jagged-1, Notch1, Notch2, Notch3, Hes-1 and Hey-1. Taken together, data from this study demonstrated that AST inhibited LEC viability, proliferation, migration and invasion, as well as fibroblastic differentiation and epithelial-mesenchymal transition process through inhibition of Jagged-1/Notch pathway, providing a potential supplemental treatment for PCO.