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Updated: Mar 22, 2026

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
Published on: September 21, 2021
Vitamin D3 attenuates oxidative stress and cognitive deficits in a model of toxic demyelination
Sepideh Tarbali1, Shiva Khezri1
1Department of Biology, Faculty of Science, Urmia University, Urmia, Iran.
Objectives:
Multiple sclerosis (MS) is a demyelinating disease. The prevalence of MS is highest where environmental supplies of vitamin D are low. Cognitive deficits have been observed in patients with MS. Oxidative damage may contribute to the formation of MS lesions. Considering the involvement of hippocampus in MS, an attempt is made in this study to investigate the effects of vitamin D3 on behavioral process and the oxidative status in the dorsal hippocampus (CA1 area) following the induction of experimental demyelination in rats.
Materials And Methods:
Animals were divided into six groups.
Control Group:
animals received no surgery and treatment; saline group: animals received normal saline; sham group: animals received 150 μl sesame oil IP; vitamin D3 group: animals received 5 μg/kg vitamin D3 IP; lysophosphatidyl choline (LPC) group (toxic demyelination's model): animals received LPC by stereotaxic intra-hippocampal injection of 2 μl LPC in CA1 area; Vitamin D3- treated group: animals were treated with vitamin D3 at doses of 5 μg/kg IP for 7 and 21 days post lesion. The spatial memory, biochemical parameters including catalase (CAT) activities and lipid peroxidation levels were investigated.
Results:
Animals in LPC group had more deficits in spatial memory than the control group in radial arm maze. Vitamin D3 significantly improved spatial memory compared to LPC group. Also, results indicated that vitamin D3 caused a decrease in lipid peroxidation levels and an increase in CAT activities.
Conclusion:
Current findings suggest that vitamin D3 may have a protective effect on cognitive deficits and oxidative stress in toxic demyelination's model.
Insights
Vitamin D3 supplementation improved spatial memory and reduced oxidative stress in a rat model of demyelination. These findings suggest vitamin D3 may protect against cognitive deficits and cellular damage in conditions like multiple sclerosis.
Area of Science:
- Neuroscience
- Neuroimmunology
- Nutritional Neuroscience
Background:
- Multiple sclerosis (MS) is a demyelinating disease associated with low vitamin D levels and cognitive deficits.
- Oxidative damage is implicated in MS lesion formation, particularly within the hippocampus.
- The hippocampus plays a crucial role in cognitive functions affected in MS.
Purpose of the Study:
- To investigate the neuroprotective effects of vitamin D3 on cognitive function and oxidative status in the hippocampus.
- To evaluate vitamin D3's impact on spatial memory and biochemical markers of oxidative stress in an experimental demyelination model.
Main Methods:
- An experimental demyelination model was induced in rats using intra-hippocampal lysophosphatidyl choline (LPC) injection.
- Animals were divided into control, sham, vitamin D3-treated, LPC-induced demyelination, and vitamin D3-treated post-LPC groups.
- Spatial memory was assessed using the radial arm maze, and biochemical parameters including lipid peroxidation and catalase activity were measured.
Main Results:
- Rats with induced demyelination exhibited significant spatial memory deficits compared to controls.
- Vitamin D3 treatment notably improved spatial memory in demyelinated rats.
- Vitamin D3 administration reduced lipid peroxidation levels and increased catalase activity, indicating reduced oxidative stress.
Conclusions:
- Vitamin D3 demonstrates a protective effect against cognitive impairment in a toxic demyelination model.
- Vitamin D3 may mitigate oxidative stress in the hippocampus, offering a potential therapeutic avenue for MS-related cognitive dysfunction.
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