Protective Effects of Nucleobinding-2 After Cerebral Ischemia Via Modulating Bcl-2/Bax Ratio and Reducing Glial Fibrillary Acid Protein Expression.
Apoptosis
Astrogliosis
Hippocampus
Ischemia
Nesfatin-1
Nucleobinding-2 (NUCB2)
Journal
Basic and clinical neuroscience
ISSN: 2008-126X
Titre abrégé: Basic Clin Neurosci
Pays: Iran
ID NLM: 101575211
Informations de publication
Date de publication:
Historique:
received:
31
05
2018
revised:
10
06
2019
accepted:
13
10
2018
entrez:
15
4
2020
pubmed:
15
4
2020
medline:
15
4
2020
Statut:
ppublish
Résumé
Nucleobinding-2 (NUCB2) or nesfatin-1, a newly identified anorexigenic peptide, has antioxidant, anti-inflammatory, and anti-apoptotic properties. Brain ischemiareperfusion induces irreversible damages, especially in the hippocampus area. However, the therapeutic effects of NUCB2 have not been well investigated in cerebral ischemia. This study was designed for the first time to investigate the protective effects of NUCB2/Nesfatin-1 on the expression of apoptosis-related proteins and reactive astrogliosis level in the CA1 area of hippocampus in an experimental model of transient global cerebral ischemia. The male Wistar rats were randomly allocated into 4 groups (sham, NUCB2, ischemia-reperfusion, and ischemia-reperfusion+NUCB21) (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 protein expression levels was performed by immunofluorescence and immunohistochemical staining. NUCB2 significantly reduced the Bax and GFAP protein levels in the CA1 area after ischemia (P<0.05). Also, NUCB2 increased Bcl-2 protein level (P<0.05). NUCB2 exerted protective effects against ischemic injury by the inhibition of astrocytes activation as an inflammatory response and decreased neuronal cell apoptosis. The present study provides the possible neuroprotective view of nesfatin-1 in the treatment of ischemia injury model in rat hippocampus.
Identifiants
pubmed: 32284834
doi: 10.32598/bcn.10.5.451
pii: bcn-10-451
pmc: PMC7149952
doi:
Types de publication
Journal Article
Langues
eng
Pagination
451-459Informations de copyright
Copyright© 2019 Iranian Neuroscience Society.
Déclaration de conflit d'intérêts
Conflict of interest The authors declared no conflict of interest.
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