Abstract
Abstract ID 100665
Poster Board 530
Purpose
There is evidence that the slow-releasing hydrogen sulfide compound, GYY 4137 (GYY) can lower intraocular pressure (IOP) in normotensive rabbits (Salvi A et al. Ocul Pharmacol Ther. 2016) and protect retinal ganglion cells (RGC) from glaucomatous loss in rats (Liu H et al., IOVS, 2017) in vivo. In the present study, we investigated the pharmacological actions of GYY on IOP and retinal degeneration in carbomer-induced ocular hypertensive (OHT), male New Zealand albino rabbits, in vivo.
Methods
OHT was induced by bilateral intracameral injection of carbomer (100 μL; 0.3%) into rabbit eyes. Acute studies: GYY (2%; 50 μL) was topically instilled into one eye while the contralateral eye received normal saline (control). IOP was assessed hourly using a pneumotonometer (Model 30 classic) until baseline IOP was attained. Chronic studies: 15 animals were divided into 3 groups (n = 5 each) and treated twice daily as follows: Group I: normotensive, saline-treated; Group II: OHT-saline treated; Group III: OHT-GYY-treated. IOP was measured daily for up to 25 days post-OHT induction. Animals were then humanely euthanized and retina isolated for morphological (H&E) and cell death (TUNEL) assays.
Results
Intracameral injection of carbomer into rabbit eyes induced OHT that was sustained for up to 25 days (maximum elevation of 123.62 ± 19.25% (p > 0.001) 9 days post-OHT induction). Acute: GYY (2%) reduced IOP up to 9 h, with a maximum reduction of 29.27 ± 5.23 % (p > 0.001) observed after 5 h. Chronic: GYY reduced IOP in the treated eye, producing a significant (p<0.05) reduction of 31.85 ± 1.47% 9 days post-OHT induction. Moreover, OHT-induced loss in RGC (18.51%; p<0.05) and Photoreceptor:Outer Nuclear Layer ratio (37.66%; p<0.001) was reduced by GYY.
Conclusion
GYY reduced IOP and protected the retina from OHT-induced damage in rabbit eyes, in vivo.
1R15EY032274-01