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一氧化氮(NO)模拟物对大鼠应激诱导的神经行为变化和脑氧化损伤的调节作用

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

作者信息

Gulati Kavita, Chakraborti Ayanabha, Ray Arunabha

机构信息

Department of Pharmacology, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi 110007, India.

出版信息

Behav Brain Res. 2007 Nov 2;183(2):226-30. doi: 10.1016/j.bbr.2007.06.018. Epub 2007 Jun 29.

Abstract

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.

摘要

本研究评估了一氧化氮(NO)模拟物对大鼠应激诱导的神经行为变化的影响以及活性氧(ROS)-活性氮(RNS)相互作用的可能参与情况。束缚应激(RS)抑制了高架十字迷宫(EPM)试验中进入开放臂的百分比和在开放臂中停留的时间。这些由RS诱导的EPM活动变化被NO模拟物L-精氨酸、硝酸异山梨酯和吗多明以不同方式减弱。暴露于RS的大鼠在这些动物的脑匀浆中表现出:(a)脂质过氧化(丙二醛,MDA)增加,以及(b)还原型谷胱甘肽(GSH)和NO代谢产物(NOx)降低。用NO模拟物预处理也以不同方式影响了RS诱导的脑氧化应激标志物变化。结果表明,NO可能预防应激诱导的脑内焦虑行为和氧化损伤,并突出了ROS-RNS相互作用的重要性。

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