Neuroprotective Effect of Magnesium Oxide/gluconate in Transient Global Cerebral Ischemia in the Rat Brain

Ischemic stroke represents a major contributor to global morbidity and mortality rates. This study aims to explore the impact of magnesium salts on oxidative stress and the degree of cerebral damage in rats subjected to transient global cerebral ischemia. The experimental procedure involved the ligation of the common carotid arteries (CCAs) for a duration of 30 minutes, followed by a 2-hour reperfusion period. The rats received magnesium (magnesium oxide/magnesium gluconate) treatment at doses of 45 or 90 mg/kg via intraperitoneal injection, administered either prior to or subsequent to the CCAs ligation. Key biomarkers, including lipid peroxidation (malondialdehyde; MDA), nitric oxide (NO), reduced glutathione (GSH), paraoxonase-1 (PON-1) activity, glial fibrillary acidic protein (GFAP), and A-beta (Aβ) peptide levels, were assessed in the brain tissue. Additionally, a histopathological analysis was conducted. In comparison to the sham-treatment group, cerebral ischemia led to a notable increase in brain malondialdehyde levels, nitric oxide alongside significant reductions in GSH and PON-1 activity. Furthermore, there was a marked elevation in brain Aβ-peptide and GFAP levels. The findings demonstrated that magnesium administration, whether prior to CCA ligation or following reperfusion, resulted in a significant reduction in lipid peroxidation, and nitric oxide, while enhancing GSH levels and PON-1 activity. Additionally, magnesium treatment significantly decreased the levels of Aβ-peptide and GFAP. Global cerebral ischemia led to neuronal degeneration, the formation of pericellular vacuoles, the presence of apoptotic cells, pyknotic nuclei, gliosis, and congestion within cerebral blood vessels. The degree of cerebral injury was mitigated by magnesium in a dose-dependent fashion. These findings indicate that magnesium administration provides neuroprotective benefits in cases of experimental global cerebral ischemia by diminishing the release of free radicals and the associated oxidative stress. It can be concluded that magnesium supplementation may serve as a beneficial adjunctive treatment for patients experiencing cerebral ischemia or those who have suffered a stroke, primarily due to its antioxidant properties.

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Publication Details

Journal
International Journal of Applied Sciences & Development
Published
2025-05-27
DOI
https://doi.org/10.37394/232029.2025.4.12
Primary Topic
Neurological Disorders and Treatments
Type
article
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article

Neuroprotective Effect of Magnesium Oxide/gluconate in Transient Global Cerebral Ischemia in the Rat Brain

Enayat A. Omara, Eman R. Youness, Omar M. E. Abdel‐Salam, Amany A. Sleem et al.
International Journal of Applied Sciences & Development
Neurological Disorders and Treatments
article

Neuroprotective Effect of Magnesium Oxide/gluconate in Transient Global Cerebral Ischemia in the Rat Brain

Enayat A. Omara, Eman R. Youness, Omar M. E. Abdel‐Salam, Amany A. Sleem, Marawan Abd El Baset
article en

Abstract

Ischemic stroke represents a major contributor to global morbidity and mortality rates. This study aims to explore the impact of magnesium salts on oxidative stress and the degree of cerebral damage in rats subjected to transient global cerebral ischemia. The experimental procedure involved the ligation of the common carotid arteries (CCAs) for a duration of 30 minutes, followed by a 2-hour reperfusion period. The rats received magnesium (magnesium oxide/magnesium gluconate) treatment at doses of 45 or 90 mg/kg via intraperitoneal injection, administered either prior to or subsequent to the CCAs ligation. Key biomarkers, including lipid peroxidation (malondialdehyde; MDA), nitric oxide (NO), reduced glutathione (GSH), paraoxonase-1 (PON-1) activity, glial fibrillary acidic protein (GFAP), and A-beta (Aβ) peptide levels, were assessed in the brain tissue. Additionally, a histopathological analysis was conducted. In comparison to the sham-treatment group, cerebral ischemia led to a notable increase in brain malondialdehyde levels, nitric oxide alongside significant reductions in GSH and PON-1 activity. Furthermore, there was a marked elevation in brain Aβ-peptide and GFAP levels. The findings demonstrated that magnesium administration, whether prior to CCA ligation or following reperfusion, resulted in a significant reduction in lipid peroxidation, and nitric oxide, while enhancing GSH levels and PON-1 activity. Additionally, magnesium treatment significantly decreased the levels of Aβ-peptide and GFAP. Global cerebral ischemia led to neuronal degeneration, the formation of pericellular vacuoles, the presence of apoptotic cells, pyknotic nuclei, gliosis, and congestion within cerebral blood vessels. The degree of cerebral injury was mitigated by magnesium in a dose-dependent fashion. These findings indicate that magnesium administration provides neuroprotective benefits in cases of experimental global cerebral ischemia by diminishing the release of free radicals and the associated oxidative stress. It can be concluded that magnesium supplementation may serve as a beneficial adjunctive treatment for patients experiencing cerebral ischemia or those who have suffered a stroke, primarily due to its antioxidant properties.

International Journal of Applied Sciences & DevelopmentVol. 4
National Research Centre (EG)
Openalex Percentile: Top 85%
Neurological Disorders and Treatments
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