Abstract
Purpose :
There is evidence that hydrogen sulfide (H2S) and endocannabinoids can protect the central nervous system against oxidative stress and glutamate-induced excitotoxicity. In the present study, we compared the neuroprotective actions of H2S (using L-cysteine as a substrate and NaHS and GYY4137 as H2S-releasing compounds) with that elicited by cannabinoids (meth-anandamide and 2-arachidonyl glycerol (2-AG)) against H2O2-induced oxidative stress in the isolated bovine retinae.
Methods :
Isolated neural retinae were pretreated with L-cysteine (10 nM - 1 µM), NaHS (30 µM -100 µM) and GYY4137 (30 µM -100 µM), or meth-anandamide (1 nM -100 nM) and 2-AG (1 µM -10 µM) for 30 minutes prior to the application of the oxidative insult with H2O2 (100 µM) for 10 minutes. Lipid peroxidation was assessed by measuring the levels of 8-isoprostane in tissues via enzyme immunoassay.
Results :
In the presence of H2O2 (100 µM), there was a 20% increase in 8-isoprostane levels in isolated retinal slices when compared to untreated controls. Pretreatment of tissues with L-cysteine, NaHS, GYY4137, meth-anadamide or 2-AG blocked the H2O2-induced increase in 8-isoprostance levels. For instance, L-cysteine (10 nM), NaHS (10 µM) and GYY4137 (100 µM) significantly (P<0.001) reversed the H2O2 (100 µM)-induced elevation in 8-isoprostane levels in the neural retina. Futhermore, meth-anandamide (1 nM) and 2-AG (3 µM) also completely prevented the H2O2 (100 µM)-induced increase in the level of the lipid peroxidation product.
Conclusions :
Both H2S-releasing compounds and cannabinoids can protect the bovine isolated neural retina from oxidative stress.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.