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As a characteristic of age-related macular degeneration (AMD), choroidal neovascularization (CNV) causes severe vision loss. The current treatment has limited efficacy. This study was to investigate effects of Salidroside against CNV and explore its underlying mechanisms. RF/6A cells were treated with 200 mM cobalt chloride (CoCl 2 ) for 6 hr to mimic hypoxic condition. Cells were then treated with Salidroside at 10, 30, and 100 µM for 24 hr. Cells treated with DMSO were used as negative control. The cell proliferation was assessed using 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium-bromid assay. The tube formation was investigated on Matrigel. The cell migration was measured by a Transwell assay. RT-qPCR was used to detect the gene expression. Immuohistochemistry and western blot were used to detect the expression of proteins. Salidroside significantly inhibited the cell migration and tube formation activity of RF/6A cells under hypoxia. Moreover, Salidroside reduced the expression levels of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1 (HIF-1) in RF/6A cells. Our data suggested that Salidroside could be a potential novel therapeutic agent against CNV.

Inhibition of hypoxia-inducible factor-1 by salidroside in an in vitro model of choroidal neovascularization