Protective effects of exogenous vitamin D on nerve injury in mice with cerebral ischemia/reperfusion.
10.12047/j.cjap.5794.2019.063
- Author:
Yong-Rong LI
1
;
Hong LI
2
Author Information
1. Department of Geriatrics, Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou 730020.
2. Shenzhen Luohu District Hospital of Traditional Chinese Medicine, Shenzhen 518001, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain;
Cytokines;
metabolism;
Infarction, Middle Cerebral Artery;
drug therapy;
Inflammation;
Male;
Mice;
Mice, Inbred C57BL;
NADPH Oxidase 2;
metabolism;
Protective Agents;
pharmacology;
Random Allocation;
Rats, Sprague-Dawley;
Reperfusion Injury;
drug therapy;
T-Lymphocytes;
Th17 Cells;
Vitamin D;
pharmacology
- From:
Chinese Journal of Applied Physiology
2019;35(4):300-303
- CountryChina
- Language:Chinese
-
Abstract:
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.
