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Mol Med Rep ; 19(2): 1032-1039, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30569139

RESUMO

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 CO­induced 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 CO­exposed 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 dose­dependent manner in the MS­treated rats compared to the positive control group, while a significant dose­dependent increase in Akt expression, a pro­survival protein, was observed. In addition, MS administration reduced pro­apoptotic 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 CO­induced cerebral injury.


Assuntos
Lesões Encefálicas/prevenção & controle , Intoxicação por Monóxido de Carbono/prevenção & controle , Monóxido de Carbono/antagonistas & inibidores , Sulfato de Magnésio/farmacologia , Necrose/prevenção & controle , Fármacos Neuroprotetores/farmacologia , Animais , Apoptose/efeitos dos fármacos , Apoptose/genética , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Lesões Encefálicas/genética , Lesões Encefálicas/metabolismo , Lesões Encefálicas/patologia , Monóxido de Carbono/toxicidade , Intoxicação por Monóxido de Carbono/genética , Intoxicação por Monóxido de Carbono/metabolismo , Intoxicação por Monóxido de Carbono/patologia , Relação Dose-Resposta a Droga , Regulação da Expressão Gênica , Injeções Intraperitoneais , Masculino , Malondialdeído/metabolismo , Necrose/genética , Necrose/metabolismo , Necrose/patologia , Estresse Oxidativo/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/genética , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ratos , Ratos Wistar , Transdução de Sinais , Proteína X Associada a bcl-2/genética , Proteína X Associada a bcl-2/metabolismo
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