| ObjectiveThe present study is to aim at systemically reseach variations of expressions ofHSP27and NF-κB protein in retina by means of the ocular trauma model. Theseare all for further exploring protective effects of Glutamine on retina cells andlaying foundation on exploiting effective therapeutic measures on retina trauma.Methods45male SD rats were obtained from Experimental Animal Center of LiaoNing Medical College.5rats were randomly obtained for normal control group.The rest40rats were made by modified Allen’s falling strike for ocular traumamodel. The successful model rats were randomly divided into model group andGln group. Each group is further divided into4groups according to the differenttimepoint (12h，24h，3d，7d),5rats per group. There is no treatment in normalgroup. The second day after retinal injury, the Gln group animals were injectedwith Gln according to0.5g/Kg per rat once a day. The model group animalswere injected with physiological saline. The retina specimen were gotten afterstopping giving Gln and physiological saline. The structural changes of eachlayer retina were observed with light microscope by means of HE staining, andthe expressions of HSP27and NF-κB were observed by immunohistochemistrystaining.Results1. Histopathologic changes of retina neuronsIn sham group, neurons were arranged orderly and intact in normal group; the neurons in model group and Gln group were swollen, arrangedasymmetrically, the cellular inter-space widened, the volume of some cellsdecreased with nulear pyknosis and dyed darkly.2. HSP27protein assayThe products of HSP27immunoreaction was brown under microscope. Innormal group, expression of HSP27protein was found in ganglion cells layerand inner nuclear layer. There was little expression for HSP27in outer nuclearlayer. The change of expression of HSP27protein was not obvious after12h inmodel group and Gln group, and there was no statistical significance comparedwith the normal group. The expression of HSP27protein obviously decreased inmodel group after24h and there was statistical significance compared with thenormal group(P<0.05). It continuously decreased and reached minimum at3day after ocular trauma. Then increased at7day, but was still lower in modelgroup than that in normal group(P<0.05). In Gln group, the change tendency ofexpression of HSP27protein was similar with model group, but it was obviouslyhigher in Gln group than that in model group at24h,3day and7day. Theaverage optical density of positive cells for HSP27protein in Gln group washigher than that inmodel group respectively(P<0.01).3. NF-κB protein assayThe products of NF-κB immunoreaction was brown under microscope.expression of NF-κB protein was found in ganglion cells layer, inner nuclearlayer, outer nuclear layer and photoreceptor cell layer. There was modestexpression of NF-κB protein in normal group. In model group, the change ofexpression of NF-κB protein was not obvious after12h, and there was nostatistical significance compared with the normal group. The expression ofNF-κB protein increased gradually and was higher in model group than that innormal group after24h(P<0.01). The expression of NF-κB protein continuouslyincreased and reached peak at3day, and then decreased at7day, but theexpression of NF-κB protein was still higher in model group than that in normalgroup(P<0.05). In Gln group. The change tendency of expression of NF-κBprotein was similar with model group, but the expression of NF-κB protein wasobviously lower in Gln group than that in model group at24h,3day and7day. The average optical density of positive cells for NF-κB protein in Gln group waslower than that in model group respectively(P<0.01).ConclusionsHSP27and NF-κB perhaps take part in pathologic process of ocular trauma;Glutamine upregulates the expression of HSP27and downregulates NF-κB onretina cells following ocular trauma, Glutamine can inhibt the apoptosis of retinacells, which maybe is the one of protective mechanism that Glutamine performits protective effcet on ocular trauma. |
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