Hydrogen sulfide prevents OGD/R-induced apoptosis via improving mitochondrial dysfunction and suppressing an ROS-mediated caspase-3 pathway in cortical neurons
Hydrogen sulfide prevents OGD/R-induced apoptosis via improving mitochondrial dysfunction and suppressing an ROS-mediated caspase-3 pathway in cortical neurons
复制标题
硫化氢通过改善线粒体功能障碍和抑制皮层神经元中 ROS 介导的 caspase-3 通路来防止 OGD/R 诱导的细胞凋亡
DOI：
10.1016/j.neuint.2013.06.004
复制
发表时间：
2013-12-01
影响因子：
4.2
通讯作者：
Wu, Jiyun
中科院分区：
文献类型：
--
作者：
Luo, Yougen;Yang, Xifei;Wu, Jiyun
硫化氢（H2S）是一种内源性气体介质，已被证明对脑缺血引起的神经元损伤具有保护作用。本研究旨在探讨H2S对OGD/R诱导的神经细胞凋亡的影响及其可能的机制。我们发现，硫氢化钠（NaHS，H2S的供体）防止OGD/R诱导的细胞内活性氧（ROS）的升高和激活的caspase-3在培养的小鼠皮层神经元。N-乙酰基-L-半胱氨酸（NAC，一种ROS清除剂）的预处理也可防止OGD/R诱导的caspase-3活化。NaHS和NAC均对抗OGD/R诱导的线粒体膜电位（MMP）下降。此外，NaHS、NAC或N-乙酰基-Asp-Glu-Val-Asp-CHO（DEVD-CHO，半胱天冬酶-3抑制剂）显示出显著抑制OGD/R诱导的神经元凋亡。这些数据表明，H2S可以通过改善线粒体功能障碍和抑制ROS激活的caspase-3信号通路来保护OGD/R诱导的神经元凋亡。皇冠版权所有（C）2013由爱思唯尔有限公司出版。保留所有权利。
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.