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Apelin-13 Inhibits Apoptosis of Cortical Neurons Following Brain Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia

Authors :
Nahid Aboutaleb
Hadi Abbaspour
Hamid Kalalian-Moghaddam
Sanaz Eftekhari
Ali Shahbazi
Mehdi Khaksari
Source :
International Journal of Peptide Research and Therapeutics. 20:127-132
Publication Year :
2013
Publisher :
Springer Science and Business Media LLC, 2013.

Abstract

Stroke is the third leading cause of death world-wide, affecting 15 million people annually. Diminished blood supply to the brain cells is the main cause of damage following stroke. When focal ischemia occurs, the core of brain tissue influenced by reduced blood supply undergoes necrotic cell death. The adipocytokine Apelin is a peptide that was isolated from a bovine stomach for the first time. This peptide and its receptor are abundantly expressed in the nervous and cardiovascular systems. According to previous studies, Apelin-13 protects cardiomyocytes from ischemic injury and apoptosis. In addition, this peptide has neuroprotective effect on hippocampal and cultured mouse cortical neurons against NMDA receptor-mediated excitotoxicity as well as cortical neurons from ischemic injury. The present study was conducted to determine whether Apelin-13 inhibits apoptosis in the ischemic penumbra in transient focal cerebral ischemia. Focal cerebral ischemia was induced in male Wistar rats by 60 min middle cerebral artery occlusion (MCAO) using a filament method, followed by 23-h reperfusion. Saline as a vehicle and Apelin-13 at doses of 50 and 100 μg were injected intracerebro-ventriculary (ICV) at the beginning of ischemia. Apoptosis and neurological dysfunction were assessed 24-h after MCAO. Our results indicated that administration of Apelin-13 at doses of 50 and 100 μg ICV markedly reduced apoptosis by decreasing positive TUNEL cells (P

Details

ISSN :
15733904 and 15733149
Volume :
20
Database :
OpenAIRE
Journal :
International Journal of Peptide Research and Therapeutics
Accession number :
edsair.doi...........1f27fb11baac09c0d0ee3f197a7c992e
Full Text :
https://doi.org/10.1007/s10989-013-9374-8