...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Biochemical and Biophysical Research Communications >Hydrogen sulfide prevents hypoxia-induced apoptosis via inhibition of an H 2O 2-activated calcium signaling pathway in mouse hippocampal neurons
【24h】

Hydrogen sulfide prevents hypoxia-induced apoptosis via inhibition of an H 2O 2-activated calcium signaling pathway in mouse hippocampal neurons

机译：硫化氢通过抑制小鼠海马神经元中的H 2O 2激活的钙信号传导途径来防止缺氧诱导的细胞凋亡

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hydrogen sulfide (H 2S), an endogenous gaseous mediator, has been shown to exert protective effects against damage to different organs in the human body caused by various stimuli. However, the potential effects of H 2S on hypoxia-induced neuronal apoptosis and its mechanisms remain unclear. Here, we exposed mouse hippocampal neurons to hypoxic conditions (2% O 2, 5% CO 2 and 93% N 2 at 37°C) to establish a hypoxic cell model. We found that 4-h hypoxia treatment significantly increased intracellular reactive oxygen species (ROS) levels, and pretreatment with NaHS (a source of H 2S) for 30min suppressed hypoxia-induced intracellular ROS elevation. The hypoxia treatment significantly increased cytosolic calcium ([Ca 2+] i), and pretreatment with NaHS prevented the increase in [Ca 2+] i. Additionally, polyethylene glycol (PEG)-catalase (a H 2O 2 scavenger) but not PEG-SOD (an O 2 - scavenger) conferred an inhibitory effect similar to H 2S on the hypoxia-induced increase in [Ca 2+] i. Furthermore, we found that pretreatment with NaHS could significantly inhibit hypoxia-induced neuronal apoptosis, which was also inhibited by PEG-catalase or the inositol 1,4,5-triphosphate (IP 3) receptor blocker xestospongin C. Taken together, these findings suggest that H 2S inhibits hypoxia-induced apoptosis through inhibition of a ROS (mainly H 2O 2)-activated Ca 2+ signaling pathway in mouse hippocampal neurons.
机译：硫化氢（H 2S）是一种内源性气态介质，已显示出对各种刺激引起的对人体不同器官的伤害的保护作用。然而，H 2 S对缺氧诱导的神经元凋亡及其机制的潜在影响仍不清楚。在这里，我们将小鼠海马神经元置于低氧条件下（在37°C下为2％O 2、5％CO 2和93％N 2）以建立低氧细胞模型。我们发现4小时缺氧治疗显着增加了细胞内活性氧（ROS）的水平，并用NaHS（H 2S的来源）预处理30分钟抑制了缺氧引起的细胞内ROS升高。低氧治疗显着增加了胞质钙（[Ca 2+] i），而NaHS预处理阻止了[Ca 2+] i的增加。另外，聚乙二醇（PEG）过氧化氢酶（H 2 O 2清除剂）而不是PEG-SOD（O 2-清除剂）对缺氧诱导的[Ca 2+] i的增加具有类似于H 2S的抑制作用。此外，我们发现用NaHS预处理可以显着抑制缺氧诱导的神经元凋亡，PEG-过氧化氢酶或肌醇1,4,5-三磷酸（IP 3）受体阻滞剂xestospongin C也可以抑制神经细胞凋亡。综上所述，这些发现表明H 2S通过抑制小鼠海马神经元中的ROS（主要是H 2O 2）激活的Ca 2+信号传导途径来抑制缺氧诱导的细胞凋亡。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号