Introduction and Background: Interleukin-1 beta (IL-1β) is a key contributor to ischemic brain injury and it is response increases permeability of the blood–brain, such that exacerbates neuronal cell death and neurological deficits. Brain ischemia-reperfusion (I/R) induces irreversible damages, especially in the hippocampus area. Nesfatin-1, a recently discovered peptide, protects dopaminergic cells against neurotoxicity with the anti-inflammatory and anti-apoptotic mechanisms. This study was designed for the first time to investigate the protective effects of Nesfatin-1 on the Interleukin-1 beta (IL-1β) protein level in the hippocampus area in an experimental model of transient global cerebral ischemia. Material and Methods: The male Wistar rats were randomly allocated into 4 groups (sham, Nesfatin-1 , ischemia-reperfusion, and ischemia-reperfusion+ Nesfatin-1) (n =7). The model of cerebral ischemia was prepared by common carotid arteries occlusion for 20 minutes. Nesfatin-1 (20 μg/kg) and saline (as a vehicle) were injected (intraperitoneally) at the beginning of the reperfusion period. The assessment of the IL-1β protein level in the hippocampus area was performed by Enzyme-linked immunosorbent assay (ELISA). Results: Nesfatin-1 significantly reduced the level of IL-1β in the hippocampal area of ischemic rats treated by Nesfatin-1, after ischemia that increased in the ischemia group compared to the sham group. Since the IL-1β is a proinflammatory cytokine that has been identified as an important mediator of neuronal cell death in cerebral ischemia. Conclusions:The result demonstrated that nesfatin-1 might suppress I/R-induced neuroinflammation via reduction IL-1β protein level. That is the time for a hard outcomes trial of inhibition IL-1β activation by Nesfatin-1 in cerebral ischemia can be promise a new treatment way.
