• Derya Özsavcí, Mehmet Erşahin, Azize Şener, Özlem Bingol Özakpinar, Hale Z Toklu, Dilek Akakín, Göksel Şener, and Berrak Ç Yeğen.
• School of Pharmacy, Department of Biochemistry, Marmara University, Istanbul, Turkey.
• Neurosurgery. 2011 Jun 1;68(6):1699-708; discussion 1708.

BackgroundThere is substantial evidence to suggest that oxidative stress plays a significant role in the development of acute brain injury after subarachnoid hemorrhage (SAH).ObjectiveTo investigate the putative neuroprotective effect of nesfatin-1, a novel peptide with anorexigenic properties, in a rat model of SAH.MethodsMale Wistar albino rats were randomly divided into control, saline-treated SAH, and nesfatin-1 (10 μg/kg IP)-treated SAH groups. To induce SAH, rats were injected with 0.3 mL blood into their cisterna magna. Forty-eight hours after SAH induction, neurological examination scores were recorded and the rats were decapitated. Brain tissue samples were taken for the determination of blood-brain barrier (BBB) permeability, brain water content, and oxidative stress markers and for histological analysis.ResultsThe neurological examination scores were increased on the second day of SAH induction. SAH resulted in impaired blood-brain barrier and edema, along with increased levels of brain tumor necrosis factor-α, interleukin-1β, interleukin-6, lipid peroxidation, protein carbonylation, and myeloperoxidase activity with concomitant decreases in antioxidant enzymes. Conversely, in the nesfatin-1-treated SAH group, SAH-induced neurological impairment and oxidative brain injury were ameliorated by nesfatin treatment. Furthermore, SAH-induced morphological changes in the basilar arteries were improved by nesfatin-1 treatment, whereas caspase-3 activity and SAH-induced elevations in the plasma levels of proinflammatory cytokines were also depressed by nesfatin-1 treatment.ConclusionThese findings suggest that nesfatin-1, which appears to have antiapoptotic and anti-inflammatory properties, exerts neuroprotection in SAH-induced injury in rats by inhibiting neutrophil infiltration and subsequent release of inflammatory mediators.Copyright © 2011 by the Congress of Neurological Surgeons

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