Visfatin Inhibits Apoptosis and Necrosis of Hippocampus CA3 Cells Following Transient Global Ischemia/Reperfusion in Rats

Visfatin, a novel adipokine, is predominantly produced by visceral adipose tissue and it has been linked to a diverse variety of cellular processes and it is an important factor in cell apoptosis and survival. Cerebral ischemia causes loss of hippocampus pyramidal cells. In this study, we investigat...

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Bibliographic Details
Published inInternational journal of peptide research and therapeutics Vol. 21; no. 2; pp. 223 - 228
Main Authors Erfani, Sohaila, Aboutaleb, Nahid, Oryan, Shahrbanoo, Shamsaei, Nabi, Khaksari, Mehdi, Kalalian-Moghaddam, Hamid, Nikbakht, Farnaz
Format Journal Article
LanguageEnglish
Published Dordrecht Springer Netherlands 01.06.2015
Springer Nature B.V
Subjects
Animal Anatomy
Apoptosis
Biochemistry
Biomedical and Life Sciences
Cellular biology
Histology
Ischemia
Life Sciences
Molecular Medicine
Morphology
Pharmaceutical Sciences/Technology
Pharmacology/Toxicology
Polymer Sciences
Rodents
Studies
Reperfusion
Ischemia
Visfatin
Hippocampus
Apoptosis
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Summary:Visfatin, a novel adipokine, is predominantly produced by visceral adipose tissue and it has been linked to a diverse variety of cellular processes and it is an important factor in cell apoptosis and survival. Cerebral ischemia causes loss of hippocampus pyramidal cells. In this study, we investigated the neuroprotective effects of visfatin in rats after global cerebral ischemia. Both common carotid arteries were occluded for 20 min followed by reperfusion. Saline as a vehicle and visfatin at doses of 100 ng were injected intracerebro-ventriculary at the time of cerebral reperfusion. Apoptosis and necrosis were assessed 96 h after ischemia. The results showed that treatment with visfatin significantly reduces apoptosis (P < 0.05) and necrotic cell death (P < 0.001) in hippocampal CA3 area, compared to the ischemia group. In conclusion, visfatin treatment, found for the first time in the present study, reduces hippocampus CA3 injuries after cerebral ischemia through preventing neuronal necrosis and apoptosis.
ISSN:1573-3149
1573-3904
DOI:10.1007/s10989-014-9449-1