METHODS: The 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, we detected the body weight and blood glucose and GC concentration of serum. The changes of retinal ganglion cell(RGC)density was investigated by HE staining. The expression of growth associated protein-43(GAP-43, a marker of neuronal axon regeneration)and synaptophysin(SYN, a marker of synaptic number)were semi-quantity analyzed by the optical density of immunofluorescence and Western blot.

RESULTS:Compared with the control group, the body weight and density of RGC and expression of SYN in diabetic group were significantly lower(P<0.01), the blood glucose and GC concentration of serum and expression of GAP-43 in diabetic group were significantly higher(P<0.01). Compared with the diabetic group, the density of RGC and expression of GAP-43, SYN in RU486 group were significantly higher(P<0.01).

CONCLUSION: Inhibition of GC could ameliorate the axonal degeneration of retinal neurons in diabetic rats, and loss of the number of synapses, and restore the RGC density of retina. The results suggest that long-term elevation of GC may be involved in the occurrence and development of diabetic retinopathy.