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CJAP ›› 2019, Vol. 35 ›› Issue (4): 300-303.doi: 10.12047/j.cjap.5794.2019.063

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Protective effects of exogenous vitamin D on nerve injury in mice with cerebral ischemia/reperfusion

LI Yong-rong1△, LI Hong 2   

  1. 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
  • Received:2018-12-12 Online:2019-07-28 Published:2019-11-06

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.

Key words: 1,25-dihydroxyvitamin D3, anti-inflammatory, ischemia/reperfusion, mice

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