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Objective: Traumatic optic neuropathy (Traumatic Optic Neuropathy, TON) is the external force moving through bone or eye passed to the indirect damage caused by the optic nerve, is a the ophthalmic common blinding one eye, this injury in blunt head trauma in about 0.5% to 5% of [1,2]. The degree of visual impairment caused by indirect traumatic optic neuropathy vary, approximately 50% of patients only light perception or no light perception vision. There is no conclusive treatment programs. With the in-depth understanding of the phenomenon of apoptosis at home and abroad in recent years a large number of optic nerve damage and repair, nerve nonrenewable view is increasingly questioned by the medical world, nerve regeneration problems, further research is expected to lead to the field of medical research and a major breakthrough. The large number of domestic and international studies have shown that drugs, surgery, gene therapy and other treatment methods have a certain role in promoting regeneration of retinal ganglion cells (Retinal Ganglion Cells, RGCs). The author through a lot of access to authoritative literature at home and abroad, learned optic nerve damage after axon regeneration is the process of a multi-link, multi-factor α2-adrenergic receptor agonist (α2-Selective Adrenergic Agonists, α2-SAs) in animals experiment confirmed the exact effect, but its specific mechanism of action remains unclear, this subject by making rat optic nerve crush in animal models, application α2-SAs (0.2% tartaric acid bromine Brimonidine) intervention, and by immunohistochemistry chemical detection rat retina bFGF, Bcl-2, Bax expression, microscopic morphology was observed by transmission electron microscopy to investigate the specific mechanism of action of the drug in the treatment of optic nerve crush in to provide new ideas, better for the clinical treatment of optic nerve damage and strategies, and enhance the understanding of nerve regeneration. Methods 90 female SD rats were randomly divided into normal group, untreated group and the treatment group and the untreated group and the treatment group using reverse tweezers forceps rat optic nerve crush in animal models, in which the treated rats made before the model and modeling to give 0.2% brimonidine tartrate eye drops, no treatment group and the normal group received no treatment. 2, respectively, after modeling l, 3,5,7,14,21 d by ketamine intramuscular anesthesia untreated group, treated rats and the corresponding time points normal rats, Abstract eye fixed in 4% paraformaldehyde solution superior temporal quadrant, cut along the equatorial region of the eye, discard the anterior segment of the eye contents, take away from the optic nerve the retinal tissue slices less than 2mm parallel HE staining, light microscope to the RGCs count to observe the dynamic changes of RGCs. 3 using the same method of anesthesia in each group at different time points for immunohistochemical staining rat, extraction eye fixed in 4% paraformaldehyde solution take the superior temporal quadrant from the optic nerve the retinal tissues bFGF less than 2mm, Bcl-2, bax immunohistochemical staining to observe the three factors in each group rat retinal expression and differences of the different time points. 4 respectively 3,7,21 d anesthesia for transmission electron microscopy three groups of rats, the rapid extraction of the eye is kept at 2.5% glutaraldehyde preservation solution, taken around the optic nerve parts retinal tissue sent to make transmission electron microscope observation of the three groups of rats retina the different periods microscopic morphological changes and differences. Results observed under a light microscope and transmission electron microscope to normal rats retina cells arranged in compact and tidy, the untreated groups retina cells arranged in irregular, the total thickness appears obvious apoptotic morphological changes, morphological changes in the treatment group compared with no treatment group significantly reduced. 2 Bcl-2 in the retina of normal rats positive reaction occurred mainly in the retinal ganglion cell layer, extend the time with injury after injury of the untreated group of Bcl-2 expression in the retina gradually increased after injury 7,14 , 21d, were strongly positive reaction; treatment group than in the untreated group was significantly increased, there is a statistically significant difference (p lt; 0.01). 3 Bax expression in the retina of normal rats, the positive reaction occurred mainly in the ganglion cell layer, inner plexiform layer, inner nuclear layer, no treatment group with optic nerve injury time to extend Bax untreated group 3,5,7 d expression in the rat retina intensity and expression intensity of the treatment group was significantly less than the untreated group, a statistically significant difference (p lt; 0.05). 4 bFGF in the retina of normal rats are mainly distributed in the retinal ganglion cell layer and inner nuclear layer, increase the intensity of staining of the the untreated group retinal ganglion cell layer and inner nuclear layer, the outer nuclear layer bFGF positive cells; treatment group than in the untreated group positive expression significantly enhanced, there is a statistically significant difference (p lt; 0.05). Conclusion 1 0.2% brimonidine tartrate the fixed eye drops significantly alleviate the the retinal morphology injury in the rat optic nerve contusion change a good effect on the rat optic nerve contusion. 0.2% tartrate brimonidine eye drops optic nerve contusion in rat retinal bFGF expression was significantly increased; increase in the expression of Bcl-2, Bax in reducing of Bcl-2/Bax ratio significantly increased, suggesting tartrate brimonidine given to the treatment of rats with optic nerve contusion mechanism may promote bFGF increased expression and inhibition of apoptosis.
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