1Department of Physiology, Faculty of Medicine, Alneelain University, Khartoum, Sudan
2Department of Biochemistry, Faculty of Medicine and Heath Sciences, Alexandria University, Alexandria, Egypt
3Department of Physiology, Faculty of Medicine, Hormozgan University of Medical Science, Bandar Abbas, Iran
4Department of Physiology – Faculty of Medicine–University of Khartoum – Khartoum, Sudan
International Journal of Clinical and Experimental Neurology.
2014,
Vol. 2 No. 2, 40-46
DOI: 10.12691/ijcen-2-2-4
Copyright © 2014 Science and Education PublishingCite this paper: Hiba A Awooda, Gihan M Sharara, Nepton Soltani, Amal M Saeed. Tumor Necrosis Factor-α and Nuclear Factor Kappa-β Expression in Rats Following Transient Focal Cerebral Ischemia Reperfusion.
International Journal of Clinical and Experimental Neurology. 2014; 2(2):40-46. doi: 10.12691/ijcen-2-2-4.
Correspondence to: Hiba A Awooda, Department of Physiology, Faculty of Medicine, Alneelain University, Khartoum, Sudan. Email:
h_alsheekh82@yahoo.comAbstract
Ischemic stroke usually initiates inflammation that potentiates neuronal death. The aim of this study was to evaluate the role of TNF-α and NF- қB in rats subjected to transient cerebral ischemia and to correlate their levels with the resulting of neurological deficits. Experimental procedures were performed on 30 adult male Wistar rats. In fifteen rats transient focal cerebral ischemia was induced by occlusion of the left common carotid artery (CCA) for 30 minutes followed by reperfusion for 24 hours (test group). Another 15 rats underwent the surgery at the same neck region without occlusion of CCA and served as a control group. Neurobehavioral assessments were evaluated. TNF-α was measured in the serum and brain tissue using ELISA method, and the expression of NF-қβ was done via western blotting as well. TNF-α concentration in both serum and brain tissue in the test group were significantly higher than control group (P < 0.001). The expression of NF- қB in the test group was significantly higher than control group (P < 0.001). Neurological deficit of the test group correlated negatively with both NF-қβ and TNF-α. Another positive correlation found between NF-қβ of the test group with the brain tissue and serum TNF-α. From the results of this study we can concluded that TNF-α and NF-қβ were significantly expressed in the affected brain tissue following cerebral ischemia/reperfusion in rats, with demonstration of a direct relationship between this inflammatory biomarkers and the consequent neurological deficits.
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