Abstract
Purpose :
Anterior ischemic optic neuropathy (AION) is ischemic damage to the optic nerve causing retinal ganglion cell (RGC) death. Currently, there is no effective treatment. The Rho-associated kinase (ROCK) is known to trigger oxidative stress, causing cell death. We use a novel ROCK inhibitor (E212) in this study to investigate the RGC survival and visual function in experimental AION.
Methods :
Adult Wistar rats were used in this study. After rAION induction the rats were immediately received an intravitreal injection of E212. The visual function and survival rate of retinal ganglion cell (RGC) was examined by using flash-VEP analysis and retrograde Fluorogold labelling four weeks after AION induction respectively. The oxidative stress was determined by using CellROX in vivo. Mann-Whitney U test was used for statistical analysis.
Results :
The P1-N2 wave shows a significantly improved in the E212 treatment group compared to PBS treated group.
(Sham 53±6 μV AION 17±6 μV E212 39±4 μV, n=6, p<0.05)
The RGC density is significantly improved by 48% in the E212 treatment group compared to PBS treated group.
(Sham 1923±143 cells, AION 645±220 cells E212 1319±160 cells, n=6, p<0.05)
CellROX intensity significantly reduced in E212 treated group compared to PBS group.
Conclusions :
E212 treatment preserves the visual function and RGC survival by reducing oxidative stress, our data suggests that Rock inhibitor has neuroprotective effects in rAIONmodel, and have future theraputic potential.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.