Metabolic Brain Disease

, Volume 34, Issue 1, pp 79–85 | Cite as

Protective effects of Nesfatin-1 peptide on cerebral ischemia reperfusion injury via inhibition of neuronal cell death and enhancement of antioxidant defenses

  • Sohaila Erfani
  • Ali Moghimi
  • Nahid AboutalebEmail author
  • Mehdi Khaksari
Original Article


Nesfatin-1 is a novel peptide with anorexigenic and anti-hyperglycemic properties. According to previous studies, this multi-functional peptide protects dopaminergic cells against neurotoxicity via anti-apoptotic effects. In addition, Nesfatin-1 protects myocardial tissue after myocardial infarction via anti-inflammatory and anti-apoptotic mechanisms. In this study, we investigated the neuroprotective effects of nesfatin-1 against cerebral ischemia reperfusion injury in the CA1 area of hippocampus in rats. 56 male Wistar rats (240-270 g) were randomly selected and allocated into four groups: (1) sham, (2) nesfatin-1, (3) ischemia/reperfusion, (4) ischemia/reperfusion+nesfatin-1. Cerebral ischemia induced by the occlusion of the common carotid arteries for 20 min was followed by reperfusion. Saline as a vehicle and nesfatin-1 (20 μg/kg) were injected intraperitoneally (IP) at the start of cerebral reperfusion. Apoptotic and necrotic cell death was detected by TUNEL and Nissl staining. Malondialdehyde (MDA) and antioxidant enzymes (GSH and SOD) levels were measured by the ELISA method. The results showed that cerebral ischemia increased the apoptotic and necrotic cell death in the CA1 area of hippocampus, while, treatment with nesfatin-1significantly reduced apoptotic and necrotic cell death. Moreover, the MDA levels of the hippocampus in ischemic rats were higher, whereas in nesfatin-1-treated rats the MDA levels were decreased. Furthermore, the SOD and GSH levels in the ischemic rats were decreased, whilst in ischemic rats treated with nesfatin-1, the SOD and GSH levels were increased. This study for the first time found that nesfatin-1 treatment improves CA1 hippocampus injuries after cerebral ischemia through preventing neuronal cell death and enhancement of antioxidant defenses.


Nesfatin-1 Apoptosis Necrosis Brain ischemia Hippocampus 



This study was supported by the grant No.95-03-130-29617from Iran University of Medical Sciences.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Sohaila Erfani
    • 1
  • Ali Moghimi
    • 2
  • Nahid Aboutaleb
    • 3
    • 4
    Email author
  • Mehdi Khaksari
    • 5
  1. 1.Department of Biology, Faculty of ScienceFerdowsi University of MashhadMashhadIran
  2. 2.Rayan Center for Neuroscience and Behavior, Department of Biology, Faculty of ScienceFerdowsi University of MashhadMashhadIran
  3. 3.Physiology Research Center, Faculty of MedicineIran University of Medical SciencesTehranIran
  4. 4.Department of Physiology, Faculty of MedicineIran University of Medical SciencesTehranIran
  5. 5.Addiction Research CenterShahroud University of Medical SciencesShahroudIran

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