...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Effect of hydrogen sulfide on intracellular calcium homeostasis in neuronal cells.
【24h】

Effect of hydrogen sulfide on intracellular calcium homeostasis in neuronal cells.

机译：硫化氢对神经元细胞内钙稳态的影响。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Hydrogen sulfide (H(2)S) is now known as a new biological mediator. In the present study, the effects of H(2)S on intracellular calcium ([Ca(2+)](i)) in neuronal SH-SY5Y cells was investigated. In SH-SY5Y neuronal cells, NaHS, a H(2)S donor, concentration-dependently increased [Ca(2+)](i). The H(2)S-induced Ca(2+) elevation was significantly attenuated by EGTA-treated calcium-free Krebs' solution. This elevation was also reduced by antagonists of L-type (verapamil and nifedipine), T-type (mibefradil) calcium channels and N-methyl-d-aspartate receptor (MK-801, AP-5 and ifenprodil). A 90% reduction in H(2)S-induced [Ca(2+)](i) elevation was found in cells pretreated with combination of all three kinds of inhibitors. Depletion of intracellular Ca(2+) store with thapsigargin or cyclopiazonic acid or blockade of ryanodine receptor with ruthenium red significantly attenuated the effect of H(2)S on [Ca(2+)](i). Inhibition of protein kinase A (PKA), phospholipase C (PLC) and protein kinase C (PKC) suppressed the H(2)S-elevated [Ca(2+)](i), suggesting that H(2)S may regulate [Ca(2+)](i) via both PKA and PLC/PKC pathways. In conclusion, it was found in this study that H(2)S increased [Ca(2+)](i) in SH-SY5Y neuronal cells by increasing Ca(2+) influx via plasma membrane and in turn releasing calcium from intracellular calcium store. The findings in the present study provide the direct evidence that H(2)S may serve as a neuromodulator.
机译：硫化氢（H（2）S）现在被称为一种新的生物介质。在本研究中，研究了H（2）S对神经元SH-SY5Y细胞内细胞内钙（[Ca（2 +）]（i））的影响。在SH-SY5Y神经元细胞，NaHS，H（2）S供体，浓度依赖性地增加[Ca（2 +）]（i）。 H（2）S诱导的Ca（2+）升高被EGTA处理的无钙克雷布斯溶液显着减弱。 L型（维拉帕米和硝苯地平），T型（米贝地尔）钙通道和N-甲基-d-天门冬氨酸受体（MK-801，AP-5和艾芬地尔）的拮抗剂也降低了这种升高。在用所有三种抑制剂组合预处理的细胞中发现H（2）S诱导的[Ca（2 +）]（i）升高了90％。 thapsigargin或cyclopiazonic酸耗尽细胞内Ca（2+）的存储，或用钌红阻断ryanodine受体，显着减弱了H（2）S对[Ca（2 +）]（i）的作用。抑制蛋白激酶A（PKA），磷脂酶C（PLC）和蛋白激酶C（PKC）抑制了H（2）S升高的[Ca（2 +）]（i），表明H（2）S可能调节[Ca（2 +）]（i）通过PKA和PLC / PKC途径。总之，在这项研究中发现，H（2）S通过增加质膜的Ca（2+）流入并反过来从细胞内释放钙，从而在SH-SY5Y神经元细胞中增加[Ca（2 +）]（i）。钙存储。在本研究中的发现提供了H（2）S可以作为神经调节剂的直接证据。

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