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Mol Med Rep ; 19(2): 1032-1039, 2019 02.
Article in English | MEDLINE | ID: mdl-30569139

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 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.


Subject(s)
Brain Injuries/prevention & control , Carbon Monoxide Poisoning/prevention & control , Carbon Monoxide/antagonists & inhibitors , Magnesium Sulfate/pharmacology , Necrosis/prevention & control , Neuroprotective Agents/pharmacology , Animals , Apoptosis/drug effects , Apoptosis/genetics , Brain/drug effects , Brain/metabolism , Brain/pathology , Brain Injuries/genetics , Brain Injuries/metabolism , Brain Injuries/pathology , Carbon Monoxide/toxicity , Carbon Monoxide Poisoning/genetics , Carbon Monoxide Poisoning/metabolism , Carbon Monoxide Poisoning/pathology , Dose-Response Relationship, Drug , Gene Expression Regulation , Injections, Intraperitoneal , Male , Malondialdehyde/metabolism , Necrosis/genetics , Necrosis/metabolism , Necrosis/pathology , Oxidative Stress/drug effects , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , Rats , Rats, Wistar , Signal Transduction , bcl-2-Associated X Protein/genetics , bcl-2-Associated X Protein/metabolism
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