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

摘要

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.