n -硝基精氨酸-甲基lester在大鼠短暂性脑缺血再灌注中的抗氧化作用。

Hiba A Awooda, Mohamed F Lutfi, Gihan M Sharara, Amal M Saeed
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引用次数: 24

摘要

背景:先前评估非选择性一氧化氮合酶(NOS)抑制剂n -硝基- l -精氨酸-甲基lester (L-NAME)在脑缺血/再灌注后的神经保护作用的报告是相互矛盾的。这项工作的目的是研究L-NAME对大鼠短暂局灶性脑缺血/再灌注的潜在益处。方法:将30只成年雄性Wistar大鼠分为3组,每组10只,第一组假手术并作为对照,缺血再灌注(I/R)组大鼠在左颈总动脉(CCA)闭塞30分钟前15分钟腹腔注射0.9%生理盐水,试验组大鼠在缺血15分钟前腹腔注射L-NAME。进行神经行为评价,定量评价血清及患脑半球丙二醛(MDA)、一氧化氮(NO)代谢物及总抗氧化能力(TAC)。结果:与对照组相比,I/R组大鼠神经功能缺损、TAC显著降低,NO、MDA显著升高(P < 0.001)。与I/R组相比,L-NAME组神经功能缺损和TAC显著改善,NO和MDA显著降低(P < 0.001)。结论:L-NAME预处理脑缺血/再灌注大鼠可显著改善神经功能缺损,同时降低脑半球氧化应激生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Role of N-Nitro-L-Arginine-Methylester as anti-oxidant in transient cerebral ischemia and reperfusion in rats.

Role of N-Nitro-L-Arginine-Methylester as anti-oxidant in transient cerebral ischemia and reperfusion in rats.

Role of N-Nitro-L-Arginine-Methylester as anti-oxidant in transient cerebral ischemia and reperfusion in rats.

Role of N-Nitro-L-Arginine-Methylester as anti-oxidant in transient cerebral ischemia and reperfusion in rats.

Unlabelled:

Background: Previous reports assessing the neuroprotective role of nonselective Nitric Oxide synthase (NOS) inhibitor N-nitro-L-arginine-methylester (L-NAME) following cerebral ischemia/reperfusion are contradictory. The aim of this work was to examine the potential benefits of L-NAME on rats subjected to transient focal cerebral ischemia/reperfusion.

Methods: The study involved 30 adult male Wistar rats divided into three groups 10 rats in each: First group was sham-operated and served as a control, a ischemia/reperfusion (I/R) group of rats infused with 0.9% normal saline intraperitoneally 15 minutes prior to 30 minutes of left common carotid artery (CCA) occlusion and a test group infused with L-NAME intraperitoneally 15 minutes prior to ischemia. Neurobehavioral assessments were evaluated and quantitative assessment of malondialdehyde (MDA), Nitric oxide (NO) metabolites and total antioxidant capacity (TAC) in both serum and the affected cerebral hemisphere were achieved.

Results: Rats' neurological deficit and TAC were significantly decreased while NO and MDA were significantly increased in the I/R compared with the control group (P < 0.001). Alternatively in the L-NAME group, neurological deficit and TAC were significantly improved while NO and MDA were significantly decreased compared to I/R group (P < 0.001).

Conclusions: L-NAME pretreatment for rats undergoing cerebral ischemia/reperfusion significantly improves neurological deficit while reducing oxidative stress biomarkers in the affected cerebral hemisphere.

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