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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 1341453, 10 pages
http://dx.doi.org/10.1155/2016/1341453
Research Article

Chronic Alcohol Intoxication and Cortical Ischemia: Study of Their Comorbidity and the Protective Effects of Minocycline

1Laboratory of Molecular Pharmacology, Institute of Biological Sciences, Federal University of Pará, 66075-110 Belém, PA, Brazil
2Laboratory of Pharmacology of Inflammation and Behavior, Institute of Health Sciences, Federal University of Pará, 66075-110 Belém, PA, Brazil
3Laboratory of Experimental Neuroprotection and Neurodegeneration, Institute of Biological Sciences, Federal University of Pará, 66075-110 Belém, PA, Brazil
4Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, 66075-110 Belém, PA, Brazil
5Department of Pharmacology, Center of Biological Sciences, Federal University of Santa Catarina, 88040-900 Florianópolis, SC, Brazil

Received 18 February 2016; Revised 4 May 2016; Accepted 19 May 2016

Academic Editor: Ruidong Ye

Copyright © 2016 Enéas Andrade Fontes-Júnior et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Chronic alcohol intoxication (CAI) increases both morbidity and mortality of stroke patients. Despite the high prevalence of CAI and ischemic stroke, studies addressing their comorbidity and/or protective alternatives remain scarce. Thus, the influence of CAI on both stroke outcome and minocycline treatment (recognized for its neuroprotective effect) was investigated. Female Wistar rats (35 days old) were treated with water or ethanol (6.5 g/kg/day, 22.5% w/v) for 55 days. Then, focal ischemia was induced by endothelin-1 in the motor cortex. Two hours later, four doses of 50 mg/kg of minocycline every 12 hours followed by five doses of 25 mg/kg every 24 hours were administered. Behavioral performance (open field and rotarod tests) and immunohistochemical (cellular density, neuronal death, and astrocytic activation) and biochemical (lipid peroxidation and nitrite levels) analyses were performed. CAI increased motor disruption, nitrite and lipid peroxidation levels, and neuronal loss caused by ischemia, whereas it reduced the astrogliosis. Minocycline was effective in preventing the motor and tissue damage caused by stroke. However, these effects were attenuated when CAI preceded stroke. Our data suggest that CAI beginning in adolescence contributes to a worse outcome in ischemic stroke survivors and reduces the benefits of minocycline, possibly requiring adjustments in therapy.