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[Protective effects of exogenous vitamin D on nerve injury in mice with cerebral ischemia/reperfusion]
1Department of Geriatrics, Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou 730020.
Objective:
To investigate the effects of 1,25-dihydroxyvitamin D3 (1,25-VitD3) supplementation on cerebral injury after ischemia/reperfusion (I/R) in mice with middle cerebral artery occlusion (MCAO).
Methods:
Male C57BL6 mice were randomly divided into Sham group, Vehicle group and 1,25-VitD3 group, with 10 mice in each group. Vehicle group and 1,25-VitD3 group were given MCAO for 1 hour, and then killed after reperfusion for 24 hours. Mice in 1,25-VitD3 group were treated with 1,25-VitD3 at the dose of 100 ng/(kg·d) by injected intraperitoneally for 5 days before MCAO operation. Cerebral ischemic penumbra areas of each group were collected for TTC staining, RT-PCR, TTC staining and immunohistochemistry assay. The function defect of mice was evaluated by using neurological function score.
Results:
Compared with the sham group, the volume of cerebral infarction in Vehicle group was increased significantly, and the expressions of IL-6, IL-1beta and Gp91phox in brain tissues were increased significantly (P＜0.05); compared with Vehicle group, supplementation of 1,25-VitD3 reduced the volume of cerebral infarction by about 50% in I/R mice (P＜0.05), and the expressions of IL-6, IL-1beta and Gp91phox in brain tissues of 1,25-VitD3 group were decreased significantly (P＜0.05). The expression of Foxp3, a T-regulatory cell marker, was significantly increased in the brain of mice (P＜0.05), while the expression of Rorc, a transcription factor, was significantly decreased (P＜0.05), suggesting that Th17/gamma Delta T-cell response was reduced and the number of neutrophils in the brain injury site of mice was significantly reduced (P＜0.05).
Conclusion:
Vitamin D could alleviate the development of cerebral infarction after arterial occlusion (MCAO) reperfusion, and its mechanism may be through regulating the inflammatory response in mouse brain I/R.
Insights
Supplementation with 1,25-dihydroxyvitamin D3 (1,25-VitD3) significantly reduced cerebral infarction volume by approximately 50% in mice after middle cerebral artery occlusion (MCAO). This neuroprotective effect is linked to the regulation of inflammatory responses in the brain.
Area of Science:
- Neuroscience
- Immunology
- Endocrinology
Background:
- Cerebral ischemia/reperfusion (I/R) injury, often caused by middle cerebral artery occlusion (MCAO), leads to significant brain damage.
- Inflammatory responses play a critical role in the pathogenesis of cerebral infarction.
- Vitamin D has demonstrated immunomodulatory properties, but its specific role in MCAO-induced brain injury requires further investigation.
Purpose of the Study:
- To investigate the neuroprotective effects of 1,25-dihydroxyvitamin D3 (1,25-VitD3) supplementation on cerebral injury following MCAO in a mouse model.
- To elucidate the potential mechanisms underlying the effects of 1,25-VitD3, focusing on inflammatory pathways.
Main Methods:
- Male C57BL6 mice underwent MCAO for 1 hour followed by 24 hours of reperfusion.
- Mice were divided into Sham, Vehicle, and 1,25-VitD3 treatment groups.
- 1,25-VitD3 was administered intraperitoneally for 5 days prior to MCAO; infarct volume, neurological scores, and inflammatory markers (IL-6, IL-1beta, Gp91phox) were assessed.
Main Results:
- MCAO significantly increased cerebral infarction volume and inflammatory markers (IL-6, IL-1beta, Gp91phox) compared to the sham group.
- 1,25-VitD3 treatment reduced infarct volume by approximately 50% and significantly decreased the expression of IL-6, IL-1beta, and Gp91phox.
- 1,25-VitD3 increased Foxp3 expression and decreased Rorc expression, indicating reduced Th17/gamma Delta T-cell responses and fewer neutrophils at the injury site.
Conclusions:
- 1,25-dihydroxyvitamin D3 (1,25-VitD3) supplementation effectively alleviates cerebral infarction development after MCAO.
- The mechanism involves the regulation of inflammatory responses in the brain, including modulation of T-cell responses and neutrophil infiltration.
- Vitamin D holds potential as a therapeutic agent for mitigating ischemic stroke injury.
