%0 Journal Article
%T Role of N-Nitro-L-Arginine-Methylester as anti-oxidant in transient cerebral ischemia and reperfusion in rats
%A Hiba A Awooda
%A Mohamed F Lutfi
%A Gihan M Sharara
%A Amal M Saeed
%J Experimental & Translational Stroke Medicine
%D 2013
%I BioMed Central
%R 10.1186/2040-7378-5-1
%X 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.NO is synthesized from its precursor L-arginine by the action of NOS and proved to be a vital cellular signaling molecule in the central nervous system [1]. Three NOS isoforms have been identified in the brain following the onset of cerebral ischemia [2]; however, their exact pathophysiological role in cerebral ischemia/reperfusion is uncertain [3,4]. NO produced by endothelial NOS (eNOS) was proved to be beneficial during cerebral ischemia/reperfusion. This is because of its vasodilator and antiplatelet effects [5]. In addition, NO increases vascular smooth muscle proliferation and migration, so enhances angiogenesis after stroke [6]. In contrast, the neuronal and inducible isoforms of NOS (nNOS, iNOS) can be neurotoxic [7], probably because they enhance peroxynitrite production, a free radical involved in lipid peroxidation, sup
%K Cerebral
%K Ischemia/reperfusion
%K L-NAME
%K Malondialdehyde
%K Nitric oxide
%K Total antioxidant capacity
%U http://www.etsmjournal.com/content/5/1/1