Objective To investigate the effects and mechanism of curcumin on the retinal neovasularization in mice with oxygeninduced retinopathy (OIR). Methods A total of 72 C57BL/6J mice were divided into normal, OIR model, vehicle control ［dimethyl sulphoxide (DMSO)］, and curcumin group (100, 50, and 10 mg). The mice in normal group lived in normoxia condition; OIR model was set up according to standard methods in the literature. Five days after OIR establishment, the mice in curcumin group received an intraperitoneal (IP) injection of 0.1 ml curcumin (100, 50, and 10 mg), and the mice in DMSO group received an IP injection of 0.1 ml 1permil; DMSO. All of the mice were executed at the age of postnatal day 17 (P17) and the eyeballs were collected. Endothelial cell nuclei breaking through the internal limiting membrane were counted after stained with hematoxylin and eosin (HE). The expression of vascular endothelial growth factor-A (VEGF-A), vascular endothelial growth factor receptor-2 (VEGFR-2), endostatin (ES), and phosphorylated p38 mitogen-activated protein kinase (p-p38MAPK) in the retina in each group were measured by real-time polymerase chain reaction (RT-PCR) and Western blot methods.Results Compared with the normal group, retinal neovascularization was found in OIR model group (P＜0.05). The number of endothelial cell nuclei was 46.00plusmn;16.00 in OIR model group and 0.17plusmn;0.41 in normal group (P＜0.05). The expression of VEGF-A, ES, and p-p38MAPK in 100 mg curcumin group differed statistically from which in 50 and 10 mg curcumin group (P＜0.05). The expression of VEGFR-2 was same in the three curcumin groups (P＞0.05). Conclusion Curcumin can inhibit the formation of retinal neovascularization; the mechanism may be associated with inhibiting the expression of VEGFA and VEGFR-2, increasing the expression of ES, and inhibiting the p38MAPK signal transduction pathway.
