| In 1995 Quigley first found that the pattern of death of retinal ganglion cells(RGCs) in glaucoma was apoptosis. Inhibiting apoptosis of RGCs is the key of neuroprotection of the optic nerve in glaucoma-tous eyes. Nitric oxide ( NO) is regarded to closely revolve in the process of apoptosis of RGCs after ischemia - reperfusion in glaucoma. Meanwhile, The detection of activated caspase - 3 is a very reliable way to identify cells destined to die by apoptosis even before many of the morphological characteristics are present. Aminoguanidine ( AG) is a kind of relatively specific inhibator of inducible nitric oxide syn-thase(iNOS). Our study aimed to discuss the effect of AG on the expression of caspase - 3 and the level of SOD, MDA and NO in rat retina after ischemia - reperfusion injury.Materials and Methods54 adlult wistar rats which weighed from 180 to 220 g were enrolled in our study and allocated to three groups; control group, ischemia - reperfusion group and drug given group. Briefly, the rats were anesthetized with intraperitoneal injections of 30mg/kg sodium pento-barbital. After topical application of 1 % dicaine, the anterior chamberwas punctured with a 5 - gauge needle connected to a bottle containing normal saline. Intraocular pressure was raised to 100 mm Hg by elevating the saline container. The infusion needle was removed from the anterior chamber 60 minutes later. Reperfusion of the retinal vascula-ture was confirmed by fundus examination. Aminoguanidine with a concentration of 100mg/kg was intraperitoneal injected in drug given group. The rats were then euthanatized at 6,24, and 72 hours after reperfusion, and their eyes were enucleated for immunohistochemistry and Estimate of the level of SOD,MDA and NO.Results1. The changes of SOD and MDA in retinaIn ischemia - reperfusion group, the expression of SOD in retina was in a lowest level at 6h after reperfusion (P <0. 01) ,and then increased along with time to the level in control group. The expression of MDA in retina was in a highest level at 6h( P <0.01) ,decreased to the level during the flowing - up period in control group.In drug given group, the level of SOD in retina was significantly higher than that in ischemia - reperfusion group( P <0. 01) , while the condition of MDA was inverse. And both of the levels were similar with control group at 24h and 72h.2. The change of NO in retinaIn ischemia - reperfusion group, the expression of NO in retina was in a highest level at 6h( P < 0. 01) ,then decreased to normal level at 72h.In drug given group, the level of NO was significantly lower than that in ischemia reperfusion group ( P < 0. 01) , and then the level ofNO was similar with the normal level.3. The expression of caspase -3 in retinaNo specific staining was detected by using the caspase - 3 antibody in the retina of control group.In ischemia - reperfusion group, there were positive staining cells in the RGCL, IPL and INL ( especially the inner part of the INL). positive staining materials were scattered in the cytoplasm with brown or light brown colors. The number of positive cells in ischenia - reperfusion group was markedly more than that in central group at 6h(P < 0. 01 ) and then decreased progressively. Compared with the control group, however, the number of positive cells was significantly different (P<0.01).In drug given group, the number of positive cells was less than that in the ischemia - reperfusion group markedly at 6h and 24h ( P < 0. 01) ,and was less than that of the ischemia - reperfusion group at 72h(P<0.05).Compared with the control group, the number of positive cells was more in drug given group, it showed significantly difference at 6h ( P < 0. 01) and difference at 24h and 72h( P < 0. 05 ) .CommentsRetinal degeneration after ischemia - reperfusion injury by transient elevation of intraocular pressure in rats shows extensive loss of neuronal elements of the retinal ganglion cell layer and the inner nuclear layer. These features closely resemble those after ret...
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