alexa Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice | OMICS International | Abstract
ISSN: 2329-6895

Journal of Neurological Disorders
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Research Article

Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice

Hania Shakil1 and Sofiyan Saleem2*
1Hamdard College of Medicine and Dentistry, Hamdard University, Sharae Madinat Al-Hikmah, Karachi 74600, Pakistan
2Del E Webb Center for Neuroscience, Aging and Stem Cell Research, Sanford Burnham Medical Research Institute, La Jolla, CA 92037, USA
Corresponding Author : Sofiyan Saleem
Del E Webb Center for Neuroscience
Aging and Stem Cell Research
Sanford Burnham Medical Research Institute
La Jolla, CA 92037, USA
Tel: 858-646-3100
Fax: 858-646-3199
E-mail: [email protected]
Received May 08, 2014; Accepted August 25, 2014; Published September 02, 2014
Citation: Shakil H, Saleem S (2014) Prostaglandin I2 IP Receptor Agonist, Beraprost, Prevents Transient Global Cerebral Ischemia Induced Hippocampal CA1 Injury in Aging Mice. J Neurol Disord 2:174. doi: 10.4172/2329-6895.1000174
Copyright: © 2014 Shakil H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Beraprost sodium is a new stable, orally active Prostaglandin I2 analogue. The aim of this study was to determine the effect of beraprost on cognitive dysfunction and locomotor impairment induced by bilateral common carotid artery occlusion in mice. We investigated the ameliorating effect of beraprost through PGI2 IP receptor by studying neurologic deficit assessment and T-maze testing in young and old male C57Bl/6 wild-type (WT) and IP receptor knockout (IP KO) mice following a 12 min bilateral common carotid artery occlusion (BCCAo) and 7 days of reperfusion. Beraprost reversed BCCAo induced cognitive impairment and neurological deficit in a dose dependent manner. Immunohistochemical studies showed attenuation of neuronal cell death, astrogliosis, microglial invasion, and myeloperoxidase (MPO) activity in both young and old WT mice after post treatment with beraprost. Moreover, after BCCAo, phosphorylated cAMP response element binding protein positive cell numbers were increased with beraprost treatment over vehicle treated controls. These results show that beraprost treatment attenuated cognitive dysfunction and neurological deficits induced by BCCAo, and suggest that this effect may be mediated by the neuroprotective effects of treatment.

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