Objective:To explore the mechanism of the inhibitory effects of FK228 on retinal nevoascularization. Methods: One-week-old C57BL/6J mice were put into the environment with 75% oxygen for 5 days to establish models of vascular proliferation retinopathy. These mice were divided into normal control

high oxygen control and treatment groups(One eye of each mouse received an intravitreal injection of 250ng of FK228

and the same volume of DMSO(dimethylsulfoxide) was injected into the other eye of the mice both in these two groups as a control). Hypoxia-inducible factor-1α(HIF-1α) and vascular endothelial growth factor(VEGF)expression were examined by immunohistochemistry. The inhibitory effects of FK228 on retinal nevoascularization were evaluated. Results:(1)There was no significant difference in HIF-1αpositive rate between normal group and treatment group(P>0.05);HIF-1αpositive rate of control groups was higher than that in normal group and treatment group with significant difference among them(P<0.05).(2)There was no significant difference in VEGF positive rate between normal group and treatment group(P>0.05);VEGF positive rate in control groups was higher than that in normal group and treatment group with significant difference among them(P<0.05). Conclusions:The mechanism of inhibitory effects of FK228 on retinal neovascularization is associated with the fact that FK228 inhibits activities of HIF-1αand deduce number of VEGF.