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Objective To establish a rat retinal ischemic reperfusion model of recombinant human erythropoietin (Recombinanthuman erythropoietin, rhEPO) on acute ocular ischemia and reperfusion in retinal ganglion cells (Retinalganglion cells, RGCs) survival and visual function recovery and its effect on inducible nitric oxide synthase (induciblenitric oxide synthase iNOS) protein expression . Explore the possibility of rhEPO on RGCs protection mechanisms. For the clinical treatment of optic nerve damage provide new ideas . Method 1 . Establish acute ocular retinal ischemia-reperfusion model , gold retrograde fluorescent tracer technique to observe ganglion cell survival , and the use of flash visual evoked potential (Flash visual evoked potential, F-VEP) were observed on visual function rhEPO recovery effect . 2 Immunohistochemical detection of acute ocular ischemia-reperfusion expression of iNOS protein and observe rhEPO on iNOS protein expression. Results 1.rhEPO 1 day after the injury , 4 days , 7 days , 14 days from RGCs survival rates were 89% , 82% , 52%, 36% to 99% , 94% , 92%, 52%. 2 , retinal ischemia reperfusion 14 days after the treatment group F-VEP amplitude of the return to normal of 71.89% in the control group returned to normal in 40.86% . Tip rhEPO ischemia-reperfusion injury to the optic nerve after recovery of visual function has a certain role in promoting. 3 no normal iNOS positive cells in the retina , one day after the injury , the retina of iNOS positive cells increased significantly, densely distributed in the outer nuclear layer of the retina , the core layer and the ganglion cell layer , four days after injury, the expression of iNOS protein has decline , there are increased expression at day 7 and continued until 14 days , rhEPO treatment group iNOS protein expression levels were significantly lower than the control group, there was a significant difference (p <0.05). Conclusion 1.rhEPO increased after ischemia-reperfusion injury in retinal ganglion cell survival , and promote the recovery of visual function . 2 ischemia-reperfusion injury , iNOS upregulation leading to apoptosis of retinal neurons one of the main ischemia-reperfusion injury after rhEPO retinal neurons can be inhibited iNOS protein expression . rhEPO on ischemia-reperfusion injury in apoptosis of retinal neurons may be through reduced iNOS expression to achieve.
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