ObjectiveTo observe the expression of CD147, matrix metalloproteinases-2 (MMP-2) and vascular endothelial growth factor (VEGF) in a rat model of oxygen induced retinopathy (OIR). MethodsEighty-four neonatal Wistar rats were divided into two groups randomly, the hyperoxia group (n=42) and the control group (n=42). Oxygen induced retinopathy was established in the hyperoxia group, the control group was raised in room air. Wholemonts were prepared from postnatal day (p) 7 and 14 rat retina to observe retinal vascular morphology. The number of endothelial cells to break through the internal limiting membrane was counted from p14 retinal paraffin sections. Expression of CD147, MMP-2 and VEGF protein levels was analyzed by immunohistochemistry on p12, p14, and p16 retinal sections. At the meantime, correlation between CD147 and MMP-2, VEGF was analyzed by two-way analysis of variance (ANOVA) test. ResultsAt p7, the retinal vasculature of the control group was radial distributed with large caliber. In OIR group, there were vasoconstriction, large area of avascular zone and a few small areas of vascular network. At p14, the normal untreated rat had interwoven retinal vasculature, but in OIR group, the retinal vasculature was expanded and tortuous, and forming lots of neovascular cluster in the boundary of the perfusion and non-perfusion regions resulting exudation and hemorrhage. At p14, the endothelial cell nuclei breakthrough the internal limiting membrane was (1.30±1.26) and (19.70±3.56) respectively in control and OIR group, the difference was statistically significant (t=21.813, P<0.01). Immunohistochemical staining showed that CD147, MMP-2, VEGF expression was low in control group but high in OIR group. From p12 to p16, CD147, MMP-2 and VEGF protein expression increased in OIR retinas compared with control samples(p12:t=5.612, 4.122, 4.955; P<0.01. p14:t=11.390, 8.047, 12.176; P<0.01. p16:t=6.355, 4.422, 5.110; P<0.01). ConclusionCD147, MMP-2 and VEGF were highly expressed in the rat model of oxygen induced retinopathy.