| Objective To study the protective effect and mechanisms of ulinastatin(UTI) to retina ischemia-reperfusion(RIR) injure.Methods Adult Wistar rates were randomly assigned to 3 groups: control, ischemia-reperfusion, ischemia-reperfusion+UTI group. The model of RIR was accomplished in Wistar adult rats by increasing the intraocular pressure to 14.3 Kp for lhour via cannulation into the anterior chamber. Rats were treated with 20000u/kg UTI at 30min before operation by intrapertoneal injected. Retinal histological changes were observes, the number of RGCs and the leukocyte infiltrating in retinal were counted, and image analysis system was usesd to detect the thickness of inner retinal layer. The expression of NF-κB and TNF-a was assessed by immunohistlchemistry.Results During the early period of RIR, the inner layer of the retina swelled and thickned, while at the later stage the decrease of RGCs number and the atrophy and thinning of nerve fiber layer were the main changer. During the early period of reperfusion, the edema of retina was reduced in treatment group than the ischemia.The inner layers of retina of retina of the treated was thicker than the untreated. The number of RGCs of treatment group was more and the number of leukocyte was less than the untreated. The expression of NF-κB and TNF-a began to increase at 6th hour and reached the peak at 24th. With the reperfusion time prolonged, it began to deceased. The expression of the treated group was relatively obvious less than the untreated.Conclusions UTI has therapeutical effect to retinal ischemia-reperfusion injure.Thepossible protective mechanism is that UTI can downregulate NF-κB expression and decrease inflammatory reaction induced by retinal ischemia-reperfusion. |