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Mol Med Rep ; 19(2): 1032-1039, 2019 02.
Artículo en Inglés | MEDLINE | ID: mdl-30569139

RESUMEN

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.


Asunto(s)
Lesiones Encefálicas/prevención & control , Intoxicación por Monóxido de Carbono/prevención & control , Monóxido de Carbono/antagonistas & inhibidores , Sulfato de Magnesio/farmacología , Necrosis/prevención & control , Fármacos Neuroprotectores/farmacología , Animales , Apoptosis/efectos de los fármacos , Apoptosis/genética , Encéfalo/efectos de los fármacos , Encéfalo/metabolismo , Encéfalo/patología , Lesiones Encefálicas/genética , Lesiones Encefálicas/metabolismo , Lesiones Encefálicas/patología , Monóxido de Carbono/toxicidad , Intoxicación por Monóxido de Carbono/genética , Intoxicación por Monóxido de Carbono/metabolismo , Intoxicación por Monóxido de Carbono/patología , Relación Dosis-Respuesta a Droga , Regulación de la Expresión Génica , Inyecciones Intraperitoneales , Masculino , Malondialdehído/metabolismo , Necrosis/genética , Necrosis/metabolismo , Necrosis/patología , Estrés Oxidativo/efectos de los fármacos , Proteínas Proto-Oncogénicas c-akt/genética , Proteínas Proto-Oncogénicas c-akt/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/genética , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Ratas , Ratas Wistar , Transducción de Señal , Proteína X Asociada a bcl-2/genética , Proteína X Asociada a bcl-2/metabolismo
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