Journal
NEUROCHEMISTRY INTERNATIONAL
Volume 63, Issue 8, Pages 826-831Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2013.06.004
Keywords
OGD/R; H2S; Apoptosis; ROS; Caspase-3
Categories
Funding
- NSFC (National Natural Science Foundation of China) [30960110, 81102154, 81100986]
- Medical Scientific Research Foundation of Guangdong Province [B2012322]
- Jiangxi Provincial Natural Science Foundation [20114BAB204015, 20132BAB205020]
- Jiangxi Provincial Educational Department Science and Technology Scheme [GJJ11531]
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Hydrogen sulfide (H2S), an endogenous gaseous mediator, has been shown to have protective effects against neuronal damage caused by brain ischemia. In this study, we explored the potential effects of H2S on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal apoptosis and the possible mechanisms. We find that sodium hydrosulfide (NaHS, a donator of H2S) prevents OGD/R-induced intracellular reactive oxygen species (ROS) elevation and activation of caspase-3 in cultured mouse cortical neurons. The pretreatment of N-acetyl-L-cysteine (NAC, an ROS scavenger) also prevents OGD/R-induced activation of caspase-3. Both NaHS and NAC counteract OGD/R-induced decline in mitochondria membrane potential (MMP). Additionally, NaHS, NAC or N-Acetyl-Asp-Glu-Val-Asp-CHO (DEVD-CHO, a caspase-3 inhibitor), is shown to significantly inhibit OGD/R-induced neuronal apoptosis. These data suggest that H2S can protect against OGD/R-induced neuronal apoptosis through improving mitochondria dysfunction and suppressing an ROS-activated caspase-3 signaling pathway. Crown Copyright (C) 2013 Published by Elsevier Ltd. All rights reserved.
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