The Study Of Nogo-66 Vaccination For Neuroprotection In Chronic High IOP Glaucoma Of SD Rats

Glaucoma is the second leading cause of blindness in the world. The pathology of glaucoma is characterized by retinal ganglial cells death and the optical fiber loss in progress. Up to now, however, there is not any effective therapy for it. Therefore, glaucoma optic nerve injury and protection have been paid more attention to by a lot of ophthalmologists.The high level of intraocular pressure is the main risk factor for glaucoma, however, the death of retinal ganglial cells and the loss of optical fiber continues to progress even if the primary cause is alleviated and removed. Now, it has been proved that there is a relationship between the immune system and RGCs survival, and enhancement protective autoimmunity (beneficial autoimmune response) can prevent neuron loss and disease progression. Recent studies have shown that the RGCs loss induced by high IOP can be reduced by vaccination with a synthetic 4-aminoacid copolymer Cop-1. Rats with high IOP were immunized with Cop-1, Schwartz found that Cop-1 could efficiently reduce RGCs loss during high IOP for 3 weeks, since a T-cell–mediated immune response could reduce RGCs loss in progress. However, Its long time action for RGCs survival with high IOP not be found, and whether Cop-1 could increase the level of serum antibody. This suggests that it is an uncertainty whether RGCs could benefit from Cop-1 in chronic high IOP.It has been confirmed that one of the reasons after the central nervous system(CNS) injury fails to survive or regenerate was myelin protein Nogo existing. C-terminal and N- terminal of Nogo are in the intramembrane, but a 66-residue of Nogo domains is being the lumenal/extracellular, called Nogo-66. It has been identified that Nogo-66 receptor (transmembrane receptor subunits) by ligand binding Nogo-66 mediating to inhibit the CNS survival or outgrowth . The level of Nogo protein increases significantly after the CNS injury, although it is low in the normal CNS, which leads to neuron apoptosis, death, or the CNS failing outgrowth.