Cognitive deficits induced by combined exposure of stress and alcohol mediated through oxidative stress-PARP pathway in the hippocampus.

Autor: Pant R; Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, Assam, India., Jangra A; Department of Pharmacology, KIET School of Pharmacy, Krishna Institute of Engineering and Technology, Ghaziabad, Uttar Pradesh, India. Electronic address: ashok.jangra@kiet.edu., Kwatra M; Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, Assam, India., Singh T; Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, Assam, India., Kushwah P; Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Guwahati, Assam, India., Bezbaruah BK; Department of Pharmacology, Gauhati Medical College, Guwahati, Assam, India., Gurjar SS; Department of Biosciences and Bioengineering, Indian Institute of Technology, Guwahati, Assam, India., Phukan S; Department of Pharmacology, Gauhati Medical College, Guwahati, Assam, India.
Jazyk: angličtina
Zdroj: Neuroscience letters [Neurosci Lett] 2017 Jul 13; Vol. 653, pp. 208-214. Date of Electronic Publication: 2017 May 30.
DOI: 10.1016/j.neulet.2017.05.058
Abstrakt: Several studies reported that stress can enhance the consumption of alcohol in humans and animals. However, the combinatorial effect of stress and alcohol on cognitive function and neurochemical alterations is quite understudied. In the present study, we have elucidated the involvement of oxidative stress-PARP cascade in alcohol and restraint stress (RS)-exposed animals using a PARP inhibitor, 1,5-isoquinolinediol (3mg/kg for 14days). Male Swiss albino mice were given alcohol (ALC) or RS (2h per day) or both in ALC+RS group for 28days. Behavioral analysis revealed cognitive dysfunction in ALC+RS group. Furthermore, oxidative stress and raised level of pro-inflammatory cytokines were found in the hippocampus region of ALC+RS group. Semi-quantitative reverse transcriptase PCR showed overactivation of PARP-1 gene in ALC+RS group. 1,5-isoquinolinediol treatment significantly prevented cognitive deficits and aforementioned neurochemical alterations. Overall, our findings showed that ALC+RS exerted deleterious effects on the hippocampus which involves oxidative stress-PARP overactivation cascade.
(Copyright © 2017 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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