[Protection of autoimmunity induced by copolymer-1 on optic nerve: experiment with rat glaucoma models]

To investigate whether copolymer-1 (Cop-1), a synthesized analogue of myelin basic protein, can protect the retina ganglion cells (RGCs) and possible mechanism thereof.

Vortex veins of rats were ligated to induce an increase of intraocular pressure (IOP) so as to establish glaucoma models. 106 rat models were randomly divided into 2 equal groups: Cop-1 Group undergoing subcutaneous injection of 200 microg Cop-1, and phosphate buffered solution (PBS) Group undergoing PBS injection as controls. Fluorogold was used to retrogradely label the RGCs. 10, 17, 24, and 31 days after the immunization some rats were killed with their eyeballs taken out. The fluorogold positive spots were calculated. Anti-rat T cell receptor (TCR) monoclonal antibody was used to mark T cells in the retina.

17, 24, and 31 days after the immunization, the RGC density of the Cop-1 Group were (2617 +/- 17)/mm(2), (2588 +/- 206)/mm(2), and (2394 +/- 15)/mm(2) respectively, all significantly higher than those of the PBS Group [(2357 +/- 37)/mm(2), (2277 +/- 340)/mm(2), and (2129 +/- 17)/mm(2) respectively, all P < 0.05]. 10, 17, 24, and 31 days after the immunization the numbers of T cells in the retina of Cop-1 Group were (11.3 +/- 2.8)/mm(2), (36.7 +/- 5.2)/mm(2), (33.9 +/- 3.0)/mm(2), and (21.4 +/- 5.9)/mm(2), all significantly higher than those of PBS Group (4.7 +/- 3.6)/mm(2), (19.7 +/- 2.4)/mm(2), (15.3 +/- 4.0)/mm(2), and (13.3 +/- 4.4)/mm(2) respectively, all P < 0.01).

Cop-1 protects RGCs. The injury of RGCs induced by increased IOP results in congregation of T cells. Cop-1 increases the number of T-lymphocyte cells congregating in the retina, which may be related to its neuroprotection.