International Journal of Clinical and Experimental Neurology
ISSN (Print): 2379-7789 ISSN (Online): 2379-7797 Website: http://www.sciepub.com/journal/ijcen Editor-in-chief: Zhiyou Cai, MD
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International Journal of Clinical and Experimental Neurology. 2014, 2(2), 24-28
DOI: 10.12691/ijcen-2-2-2
Open AccessReview Article

Tumor Necrosis Factor-α in Rats Following Transient Focal Cerebral Ischemia Reperfusion and Its Relation to Oxidative Stress

Hiba A Awooda1, , Gihan M Sharara2 and Saeed A Mahmoud3

1Department of Physiology, Faculty of Medicine and Heath Sciences, Alneelain University, Khartoum, Sudan

2Department of Biochemistry, Faculty of Medicine and Heath Sciences, Alexandria University, Alexandria, Egypt

3Department of Physiology, Faculty of Medicine and Heath Sciences, University of Khartoum, Khartoum, Sudan

Pub. Date: November 06, 2014

Cite this paper:
Hiba A Awooda, Gihan M Sharara and Saeed A Mahmoud. Tumor Necrosis Factor-α in Rats Following Transient Focal Cerebral Ischemia Reperfusion and Its Relation to Oxidative Stress. International Journal of Clinical and Experimental Neurology. 2014; 2(2):24-28. doi: 10.12691/ijcen-2-2-2

Abstract

Background: The role of TNF-α in ischemic/reperfusion (I/R) is still controversial. The aim of this study was to assess TNF-α in rats subjected to transient cerebral I/R and to correlate their levels with the resulting neurological deficits and oxidative stress biomarkers malondialdehyde and total antioxidant capacity (TAC). Material and Method: Experimental procedures were performed on 30 adult male Wistar rats. Divided into two groups fifteen rats in each, test group subjected to transient focal cerebral I/R by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24-hours. A control group underwent the surgery at the same neck region without occlusion of the CCA. Neurobehavioral assessments were evaluated. TNF-α was measured using ELISA method. Malondialdehyde and TAC were estimated colorimetry. Results: In the test group TNF-α and Malondialdehyde concentration in both serum and brain tissue were significantly higher than control group (P =0.000). In contrast, the serum and brain tissue levels of TAC in the test group was significantly lower compared to the sham operated rats (P = 0.000). The brain tissue and serum level of TNF-α were correlated negatively with neurological deficit and TAC and positively with Malondialdehyde (P = 0.000). Conclusion: the present study revealed a potential injurious role of TNF-α in rats subjected to cerebral I/R and demonstrated a direct relationship between TNF-α and oxidative stress biomarkers and the consequent neurological deficits.

Keywords:
cerebral ischemia/reperfusion TNF-α malondialdehyde and total antioxidant capacity

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