Magnesium sulfate ameliorates carbon monoxide-induced cerebral injury in male rats

Bagheri, G. and Rezaee, R. and Tsarouhas, K. and Docea, A. O. and Shahraki, J. and Shahriari, M. and Wilks, M. F. and Jahantigh, H. and Tabrizian, K. and Moghadam, A. A. and Bagheri, S. and Spandidos, D. A. and Tsatsakis, A. and Hashemzaei, M. (2019) Magnesium sulfate ameliorates carbon monoxide-induced cerebral injury in male rats. Molecular Medicine Reports, 19 (2). pp. 1032-1039.

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Abstract

Carbon monoxide (CO) has been shown to induce several cardiovascular abnormalities, as well as necrosis, apoptosis and oxidative stress in the brain. Magnesium sulfate (MS) has been shown to have beneficial activities against hypoxia in the brain. In the present study, the possible protective effects of MS against CO-induced cerebral ischemia were investigated. For this purpose, 25 male Wistar rats were exposed to 3,000 ppm CO for 1 h. The animals were divided into 5 groups (n=5 in each group) as follows: The negative control group (not exposed to CO), the positive control group (CO exposed and treated with normal saline), and 3 groups of CO-exposed rats treated with MS (75, 150 and 300 mg/kg/day) administered intraperitoneally for 5 consecutive days. On the 5th day, the animals were sacrificed and the brains were harvested for the evaluation of necrosis, apoptosis and oxidative stress. Histopathological evaluation revealed that MS reduced the number and intensity of necrotic insults. The Bax/Bcl2 ratio and malondialdehyde (MDA) levels were significantly decreased in a dose-dependent manner in the MS-treated rats compared to the positive control group, while a significant dose-dependent increase in Akt expression, a pro-survival protein, was observed. In addition, MS administration reduced pro-apoptotic indice levels, ameliorated histological insults, favorably modulated oxidative status and increased Akt expression levels, indicating a possible neuroprotective effect in the case of CO poisoning. On the whole, the findings of this study indicate that MS may prove to be useful in protecting against CO-induced cerebral injury. © 2019 Spandidos Publications. All rights reserved.

Item Type: Article
Additional Information: Cited By :4 Export Date: 16 February 2020 Correspondence Address: Tsatsakis, A.; Department of Forensic Sciences and Toxicology, Faculty of Medicine, University of Crete, VoutesGreece; email: aris@med.uoc.gr
Uncontrolled Keywords: Akt Apoptosis Bax/Bcl2 ratio Carbon monoxide poisoning Cerebral ischemia Magnesium sulfate Malondialdehyde Necrosis Oxidative stress beta actin carbon monoxide carboxyhemoglobin malonaldehyde protein Bax protein bcl 2 protein kinase B Bax protein, rat Bcl2 protein, rat neuroprotective agent Akt signaling animal experiment animal model animal tissue Article brain hypoxia brain injury brain ischemia brain necrosis brain tissue carbon monoxide intoxication clinical evaluation controlled study drug efficacy drug mechanism histopathology male neuroprotection neurotoxicity nonhuman protein expression level rat survival factor animal antagonists and inhibitors brain dose response drug effect gene expression regulation genetics intraperitoneal drug administration metabolism pathology signal transduction Wistar rat Animals bcl-2-Associated X Protein Brain Injuries Dose-Response Relationship, Drug Injections, Intraperitoneal Neuroprotective Agents Proto-Oncogene Proteins c-akt Proto-Oncogene Proteins c-bcl-2 Rats Rats, Wistar
Subjects: QV pharmacology
Divisions: Mashhad University of Medical Sciences
Depositing User: mr lib1 lib1
Date Deposited: 20 Jun 2020 09:17
Last Modified: 20 Jun 2020 09:17
URI: http://eprints.mums.ac.ir/id/eprint/18275

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