Abstract of research

BIOCHEMICAL STUDYING ON EXPERMENTAL ACUTE BRAIN STROKE

Omayma A. Ragab, Hussein, S.A. and Asmaa A. Elwakil

Abstract

In the present study, biochemical abnormalities and oxidative mechanisms of focal cerebral ischemia induced by using left common carotid artery occlusion (LCCAO) model of brain stroke in rats were evaluated. Male rats (n=70) were divided into five groups: Group I (Control; n=6) without LCCAO. Group II, III, IV and V (n=16 per each) submitted to ½, 1, 4, 6 hours occlusion of LCCA, respectively and the filament was retracted thereafter to allow the reperfusion of the ischemic region. Blood samples and tissue specimens (brain) were collected from all animals at 0, 1, 3 and 24 hours after reperfusion. Samples in control group were collected once only. L-malondialdehyde (L-MDA), creatin kinase (CK) and C-reactive protein (CRP) were determined in sera. L-MDA, nitric oxide (NO), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), actylecholinestraes (AChE), lactate dehydrogenase (LDH), lactic acid and sodium (Na+) were determined in brain tissues as well as fibrinogen concentration in plasma. Results revealed that LCCA occlusion in male rats significantly increased the levels of brain L-MDA, lactate, sodium, GPx SOD, AChE, LDH and plasma fibrinogen, and significantly decreased brain NO and CAT and serum Ck and C-RP as compared to control rats. Reperfusion of LCCA after 24 hours significantly increased brain L-MDA, GPx, CAT and SOD, and serum C-RP with a significant decrease in brain NO, sodium, AchE, and serum Ck as well as fluctuation in brain LDH, lactate and plasma fibrinogen levels as compared to zero-hour readings. This study provided evidence that brain ischemia has a harmful effect on brain energy metabolism and induced an oxidative stress via production of rapid increase in the generation of reactive oxygen species, rise in lipid peroxidation and disrupted enzymatic antioxidant defenses.