首页> 外文期刊>Behavioural Brain Research: An International Journal >Modulation of stress-induced neurobehavioral changes and brain oxidative injury by nitric oxide (NO) mimetics in rats.
【24h】

Modulation of stress-induced neurobehavioral changes and brain oxidative injury by nitric oxide (NO) mimetics in rats.

机译:一氧化氮(NO)模拟物对应激诱导的神经行为变化和脑氧化损伤的调节。

获取原文
获取原文并翻译 | 示例
           

摘要

The present study evaluated the effects of NO mimetics on stress-induced neurobehavioral changes and the possible involvement of ROS-RNS interactions in rats. Restraint stress (RS) suppressed both percent open arm entries and time spent in the open arms in the elevated plus maze (EPM) test. These RS-induced changes in EPM activity were attenuated by the NO mimetics, l-arginine, isosorbide dinitrate and molsidomine, in a differential manner. RS-exposed rats showed (a) increased lipid peroxidation (MDA) and (b) lowered reduced glutathione (GSH) and NO metabolites (NOx), in brain homogenates of these animals. Pretreatment with the NO mimetics also differentially influenced RS-induced changes in brain oxidative stress markers. The results suggest that NO may protect against stress-induced anxiogenic behavior and oxidative injury in the brain and highlight the significance of ROS-RNS interactions.
机译:本研究评估了NO模拟物对应激诱导的神经行为改变的影响以及大鼠中ROS-RNS相互作用的可能参与。约束压力(RS)抑制了高架迷宫(EPM)测试中张开双臂的进入百分比和张开双臂所花费的时间。这些RS诱导的EPM活性变化被NO模拟物,1-精氨酸,硝酸异山梨酯和莫斯多明以不同的方式减弱。暴露于RS的大鼠在这些动物的脑匀浆中显示(a)脂质过氧化(MDA)增加和(b)降低的谷胱甘肽(GSH)和NO代谢产物(NOx)降低。用NO模拟物进行预处理还可以不同程度地影响RS诱导的脑氧化应激标记物的变化。结果表明,NO可以防止应激引起的焦虑行为和大脑中的氧化损伤,并突出了ROS-RNS相互作用的重要性。

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