Down-Regulation of Tumour necrosis factor-α by Nucleobinding-۲in Animal Model of Cerebral Ischemia

Introduction: Tumor necrosis factor alpha (TNFα) is a brain and systemically generated cytokine. TNFαplays an important role in acute inflammatory responses, and it is suspected to exacerbate strokepathology. Nucleobinding-۲ (NUCB۲) or nesfatin-۱, a newly identified anorexigenic peptide, hasantioxidant, anti-inflammatory properties. In this study, the protective effects of Nucleobinding-۲ on theTNFα protein level in the hippocampus area in experimental model of transient global cerebral ischemiawas investigated.Material and Methods: ۲۸ male Wistar rats were randomly allocated into ۴ groups (sham, NUCB۲,ischemia-reperfusion, and ischemia-reperfusion+NUCB۲۱) (n =۷). The model of cerebral ischemia wasprepared by common carotid arteries occlusion for ۲۰ minutes. NUCB۲ (۲۰ μg/kg) and saline (as avehicle) were injected (intraperitoneally) at the beginning of the reperfusion period. The assessment of theTNFα protein level in the hippocampus area was performed by Enzyme-linked immunosorbent assay(ELISA).Results: Results demonstrated that Nucleobinding-۲ significantly regulates the level of TNFα protein inthe hippocampal area of ischemic rats treated by NUCB۲.Conclusions: We highlight the key findings in the regulation of signaling cascades inflammatory responserelated to TNFα expression by Nucleobinding-۲. This can be the novel promising therapeutic target forimproved treatment of ischemic damage caused by brain ischemia.

Keywords:

Nucleobinding-۲ , brain ischemia , anti-inflammatory , TNFα