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چکیده
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Introduction: Tumor necrosis factor alpha (TNFα) is a brain and systemically generated cytokine. TNFα plays an important role in acute inflammatory responses, and it is suspected to exacerbate stroke pathology. Nucleobinding-2 (NUCB2) or nesfatin-1, a newly identified anorexigenic peptide, has antioxidant, anti-inflammatory properties. In this study, the protective effects of Nucleobinding-2 on the TNFα protein level in the hippocampus area in experimental model of transient global cerebral ischemia was investigated. Material and Methods: 28 male Wistar rats were randomly allocated into 4 groups (sham, NUCB2, ischemia-reperfusion, and ischemia-reperfusion+NUCB21) (n =7). The model of cerebral ischemia was prepared by common carotid arteries occlusion for 20 minutes. NUCB2 (20 μg/kg) and saline (as a vehicle) were injected (intraperitoneally) at the beginning of the reperfusion period. The assessment of the TNFα protein level in the hippocampus area was performed by Enzyme-linked immunosorbent assay (ELISA). Results: Results demonstrated that Nucleobinding-2 significantly regulates the level of TNFα protein in the hippocampal area of ischemic rats treated by NUCB2. Conclusions: We highlight the key findings in the regulation of signaling cascades inflammatory response related to TNFα expression by Nucleobinding-2. This can be the novel promising therapeutic target for improved treatment of ischemic damage caused by brain ischemia.
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