AIM:To investigate the role of adiponectin(APN)in C57BL/6J mice model of oxygen-induced retinopathy(OIR).

METHODS: Neonatal C57BL/6J mice were divided randomly into three groups: normoxic control group, physiological saline injection of OIR group and adiponectin injection of OIR group. The mice of the latter two groups were exposed to 75%±2% oxygen from 7d(P7)～P12 to induced OIR. Recombinant APN(rAPN)was injected intraperitoneally(i.p., 3.0μg/g)in a mice model of OIR from P7～P15. Another set of mice model of OIR were received a similar treatment with physiological saline. All eyes were collected at P17. The right eyes were whole mounted and stained with Lectin to observe central retinal avascular area and the growth of pathological neovascularization; The left eyes were performed histopathological cross sections stained with HE to analyzed the histopathological changes in the retina. The eyes were enucleated to assess the levels of reactive oxygen species(ROS)and NO. The protein expression of iNOS, nNOS, eNOS were detected by Western-blot.

RESULTS: The central retinal avascular area, neovascular area were markedly decreased after the APN injection compared with physiological saline injection of OIR group(t=7.304, P<0.01; t=2.654, P<0.01). Compared with physiological saline injection of OIR group, the levels of ROS were lower(t=13.349, P<0.01), the levels of NO were higher(t=3.023, P<0.01), the expression of iNOS were decreased(t=5.112, P<0.01), the expression of eNOS were decreased(t=7.421, P<0.01). nNOS expression had no significant difference(t=1.074, P>0.01).

CONCLUSION:The realtus demonstrate that APN can promote physiological NO by acting endogenous eNOS, while suppress ROS/RNS generation and play a protective role in retinal vessels in OIR process.