Abstract
Purpose We sought to explore the effects of intravitreal injection of the Rho-kinase inhibitor Y-27632 in a rodent model of nonarteritic anterior ischemic optic neuropathy (rAION). Methods The rAION model was established by using laser-induced photoactivation of intravenously administered Rose Bengal in rats. The rats received intravitreal injections of Y-27632 or PBS 1, 3, and 6 days after rAION induction. Optical coherence tomography (OCT) was performed at 2 days and 4 weeks after induction. Visual evoked potential (VEP) was used to evaluate the visual function at 4 weeks. Brn3a immunofluorescence staining of surviving RGCs and apoptosis assays of RGCs were performed at 4 weeks. Results Optic nerve head (ONH) width was significantly reduced in the Y-27632 group compared with that in the PBS group at 2 days after induction (p < 0.05). At 4 weeks, the P1 amplitude of flash-VEP (FVEP) in the Y-27632 group was significantly higher than that of the PBS group (p < 0.05). The RGC densities in the central and midperipheral retinas in the Y-27632 group were significantly higher than those in the PBS group (p < 0.05). Furthermore, there was a significant decrease in apoptotic RGCs in the Y-27632 group than in the PBS group (p < 0.05). Conclusions Intravitreal injection of Y-27632 had neuroprotective effects on ONH edema, RGC survival, and visual function preservation in rAION.
Highlights
Nonarteritic anterior ischemic optic neuropathy (NAION) is the leading cause of sudden optic nerve-related vision loss in elderly people [1]
Two days after rodent models of AION (rAION) induction, standard deviation (SD)-Optical coherence tomography (OCT) revealed that the Optic nerve head (ONH) width in the sham, phosphatebuffered saline (PBS)-treated, and Y-27632-treated groups were 357.2 ± 24.1 μm, 574.4 ± 53.6 μm, and 454.4 ± 51.2 μm, respectively
Our findings in this study demonstrated for the first time that intravitreal injection of the Rho-associated protein kinase (ROCK) inhibitor Y-27632 can effectively exert neuroprotective effects in rAION, as evidenced by FVEP analysis and the preservation of retinal ganglion cells (RGCs)
Summary
Nonarteritic anterior ischemic optic neuropathy (NAION) is the leading cause of sudden optic nerve-related vision loss in elderly people [1]. Primate and rodent models of NAION have been established to facilitate exploration of the underlying mechanisms as well as identification of potential therapies [2,3,4,5]. In these models, a laser is used to activate an intravascular photoactive dye to produce superoxide radicals, which causes capillary thrombosis of the anterior optic nerve and secondary apoptosis of retinal ganglion cells (RGCs) [2]. Studies show that observable optic nerve changes in rodent models of AION (rAION) and primate NAION (pNAION) are similar to the clinical changes observed in human NAION, including optic disc edema, electrophysiological changes, and axonal involvement [2,3,4]
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