Neuroprotective role of Nesfatin-۱ via modulating level of IL-۱βafter cerebral ischemia in rat

سال انتشار: 1401
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 100

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شناسه ملی سند علمی:

BIOLOGY05_078

تاریخ نمایه سازی: 19 اردیبهشت 1402

چکیده مقاله:

Introduction and Background: Interleukin-۱ beta (IL-۱β) is a key contributor to ischemic brain injuryand it is response increases permeability of the blood–brain, such that exacerbates neuronal cell death andneurological deficits. Brain ischemia-reperfusion (I/R) induces irreversible damages, especially in thehippocampus area. Nesfatin-۱, a recently discovered peptide, protects dopaminergic cells againstneurotoxicity with the anti-inflammatory and anti-apoptotic mechanisms. This study was designed for thefirst time to investigate the protective effects of Nesfatin-۱ on the Interleukin-۱ beta (IL-۱β) protein levelin the hippocampus area in an experimental model of transient global cerebral ischemia.Material and Methods: The male Wistar rats were randomly allocated into ۴ groups (sham, Nesfatin-۱,ischemia-reperfusion, and ischemia-reperfusion+ Nesfatin-۱) (n =۷). The model of cerebral ischemia wasprepared by common carotid arteries occlusion for ۲۰ minutes. Nesfatin-۱ (۲۰ μg/kg) and saline (as avehicle) were injected (intraperitoneally) at the beginning of the reperfusion period. The assessment of theIL-۱β protein level in the hippocampus area was performed by Enzyme-linked immunosorbent assay(ELISA).Results: Nesfatin-۱ significantly reduced the level of IL-۱β in the hippocampal area of ischemic ratstreated by Nesfatin-۱, after ischemia that increased in the ischemia group compared to the sham group.Since the IL-۱β is a proinflammatory cytokine that has been identified as an important mediator ofneuronal cell death in cerebral ischemia.Conclusions:The result demonstrated that nesfatin-۱ might suppress I/R-induced neuroinflammation viareduction IL-۱β protein level. That is the time for a hard outcomes trial of inhibition IL-۱β activation byNesfatin-۱ in cerebral ischemia can be promise a new treatment way.

نویسندگان

Sohaila Erfani

Ph.D of Animal Physiology, Faculty of Science, Ilam University

Ali Moghimi

Department of Physiology, Faculty of Medicine, Physiology Research Center, Iran University ofMedical Sciences, Tehran, Iran.