Awooda Hiba A, Lutfi Mohamed F, Sharara Gihan M, Saeed Amal M
Department of Physiology - Faculty of Medicine and Heath Sciences, Alneelain University, Khartoum, Sudan.
Exp Transl Stroke Med. 2013 Jan 4;5(1):1. doi: 10.1186/2040-7378-5-1.
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.
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.
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).
L-NAME pretreatment for rats undergoing cerebral ischemia/reperfusion significantly improves neurological deficit while reducing oxidative stress biomarkers in the affected cerebral hemisphere.
先前评估非选择性一氧化氮合酶(NOS)抑制剂N-硝基-L-精氨酸甲酯(L-NAME)在脑缺血/再灌注后神经保护作用的报告相互矛盾。本研究的目的是探讨L-NAME对短暂性局灶性脑缺血/再灌注大鼠的潜在益处。
该研究纳入30只成年雄性Wistar大鼠,分为三组,每组10只:第一组为假手术组,作为对照;第二组为缺血/再灌注(I/R)组,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;第三组为试验组,在缺血前15分钟腹腔注射L-NAME。进行神经行为学评估,并对血清和受影响的脑半球中的丙二醛(MDA)、一氧化氮(NO)代谢产物和总抗氧化能力(TAC)进行定量评估。
与对照组相比,I/R组大鼠的神经功能缺损和TAC显著降低,而NO和MDA显著升高(P < 0.001)。与I/R组相比,L-NAME组的神经功能缺损和TAC显著改善,而NO和MDA显著降低(P < 0.001)。
对脑缺血/再灌注大鼠进行L-NAME预处理可显著改善神经功能缺损,同时降低受影响脑半球的氧化应激生物标志物水平。