Effect Of Glucocorticoids On The Regeneration Of Retinal Neurons In Diabetic Rats

ObjectiveTo investigate the detrimental effect of glucocorticoid(GC)on the retinal neurons of diabetes mellitus(DM)rats.MethodsThe DM model was induced by intraperitoneal injection(IP)of streptozotocin in adult male rats,and the solution of RU486 was configured with dimethyl sulfoxide(DMSO).RU486 treatment group with glucocorticoid receptor antagonist RU486 and diabetic group with DMSO by intraperitoneal injection was in successful DM model.Naive rats were injected with DMSO as control group.Three months later,the body weight,blood glucose,serum glucocorticoid concentration,MDA content and SOD activity were evaluated.Retinal ganglion cell density was calculated by HE staining.The expression of GAP-43(axonal regeneration related markers)and SYN(a marker of synaptic number)and Caspase-3(a marker of apoptosis)were semi-quantity analyzed by the optical density of immunofluorescence and Western blot.ResultsThere was no significant difference in the body weight and blood glucose between the groups(P > 0.05).Compared with the control group,the body weight of diabetic group and RU486 treatment group was significantly lower(P< 0.01),and the blood glucose was significantly higher(P < 0.01)after three months.GC concentration test results showed,compared with the control group,GC concentration of serum in the diabetic group was significantly higher(P <0.01),and there was no significant difference between RU486 treatment group and diabetic group(P > 0.05).MDA results showed that compared with the control group,the content of MDA in the diabetic group was significantly higher(P < 0.01),and the RU486 treatment group was significantly lower than that of the diabetic group(P <0.01).SOD activity assay showed that compared with the control group,the SOD activity was significantly lower in the diabetic group(P < 0.01),and the RU486 treatment group was significantly higher than that of the diabetic group(P < 0.01).HE staining showed that the RGC of control group was single layer and complete morphology and diabetic group was disorder and irregular shape,lower density than the control group(P < 0.01).The RGC density in the RU486 treatment group was significantly higher than that in the diabetic group(P <0.01).GAP-43 immunofluorescence showed that GAP-43 was only expressed in the inner plexiform layer in the control group,but also in the diabetic and RU486 treated group.The results of optical density analysis showed that compared with the control group,the diabetic group(P < 0.01)increased significantly in the RU486 group(P < 0.01).SYN was mainly expressed in the inner plexiform layer and outer plexiform layer,the analysis results show the value of optical density,compared with the control group,diabetic group decreased significantly(P < 0.01),compared with the diabetic group,RU486 treatment group increased significantly(P < 0.01).The results of Western blot showed that the expression of GAP-43 in the control group was significantly increased in the diabetic group(P < 0.01),while that in the RU486 treatment group was significantly increased(P < 0.01).Compared with the control group,the expression of SYN in diabetic group was significantly decreased(P < 0.01),and SYN expression was significantly increased in the RU486 group(P < 0.01).The expression of Caspase-3showed that the expression of protein in diabetic group was significantly higher than that of control group(P < 0.01),and RU486 treatment group was significantly lower than that of control group(P < 0.01).ConclusionInhibition of GC can promote the regeneration of retinal neurons in diabetic rats,and has protective effects on damaged RGC in DR.