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

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.

Triacontanoic ester of 5ʹʹ-hydroxyjustisolin: Tumour suppressive role in cervical cancer via Bcl-2, BAX and caspase-3 mediated signalling

“…The BAX/Bcl-2 ratio is considered a measure of cell susceptibility to apoptosis [28] as well as proapoptotic index [29]. This ratio was found to be significantly decreased in the current study as reported earlier and may be due to the increased apoptosis via increasing proapoptotic Bax and decreasing antiapoptotic Bcl-2 expression in an animal model [30,31].…”

Therapeutic effect and molecular mechanism of Salvia Miltiorrhiza on rats with acute brain injury after carbon monoxide poisoning based on the strategy of internet pharmacology

“…COP leads to inhibition of O 2 transport and development of tissue hypoxia, which in turn causes cell apoptosis 49 . Due to the nonrenewability of neurons, some scholars believe that apoptosis is an important pathogenesis of brain injury caused by COP 23,50 . Jurič et al found that carbon monoxide decreased the activity of astrocyte cells, increased the reactive oxygen species, and reduced the mitochondrial membrane potential and intracellular ATP level.…”

CGA ameliorates cognitive decline by regulating the PI3K/AKT signaling pathway and neurotransmitter systems in rats with multi-infarct dementia

“…Worldwide, vascular dementia is the second most common form of dementia accompanied by obvious cognitive dysfunction after Alzheimer's disease ( 29 ), and MID is a common type of vascular dementia. Currently, no licensed drugs are available for the treatment of vascular dementia ( 30 ), and the reported therapeutic strategies for the disease primarily focus on inhibiting oxidative stress, apoptosis and inflammation ( 31 , 32 ). Multiple and cortical microinfarctions are closely related to dementia and cognition ( 33 ), which is associated with their direct influence on the production of ATP in the brain ( 7 ).…”