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中国应用生理学杂志 ›› 2019, Vol. 35 ›› Issue (4): 300-303.doi: 10.12047/j.cjap.5794.2019.063

• 研究论文 • 上一篇    下一篇

外源性维生素D对小鼠脑缺血/再灌注神经损伤的保护作用*

李永荣1△, 李红2   

  1. 1. 甘肃中医药大学附属医院老年病科, 兰州 730020;
    2. 深圳市罗湖区中医院, 深圳 518001
  • 收稿日期:2018-12-12 出版日期:2019-07-28 发布日期:2019-11-06
  • 通讯作者: ,Tel: 13893358576 ; E-mail: rongbaobao1215@163.com
  • 基金资助:
    *国家自然科学基金(81560743)

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

摘要: 目的:观察小鼠大脑中动脉闭塞(MCAO)模型制备前5 d 连续补充1,25-二羟维生素D3(1,25-VitD3)对缓解小鼠缺血/再灌注(I/R)后脑损伤中的作用。方法:雄性C57BL6小鼠随机分为Sham组、Vehicle组和1,25-VitD3组,每组10只小鼠;Vehicle组和1,25-VitD3组小鼠均进行大脑MCAO1 h,再灌注24 h后处死小鼠,1,25-VitD3组MCAO手术前5 d连续腹腔注射,100 ng/(kg·d);取各组小鼠脑缺血半影区,进行TTC染色、RT-PCR及免疫组化检测,采用神经功能评分评估小鼠功能缺陷。结果:与sham组相比,Vehicle组小鼠脑梗死体积明显增加,小鼠脑组织中促炎介质IL-6、IL-1β和Gp91phox表达均明显增高(P<0.05);与Vehicle组相比,补充1,25-VitD3可减少I/R小鼠大约50%梗死体积(P<0.05), 1,25-VitD3组小鼠脑组织中IL-6、IL-1β和Gp91phox表达明显降低(P<0.05),小鼠脑内T调节细胞标志物Foxp3 mRNA表达明显升高(P<0.05),而转录因子Rorc mRNA表达明显较低(P<0.05),提示Th17/γδT细胞反应减少,小鼠脑损伤部位中性粒细胞数量明显降低(P<0.05)。结论:维生素D可以缓解动脉闭塞(MCAO)再灌注脑梗死发展,其机制可能是通过调节小鼠脑I/R中炎症反应。

关键词: 1,25-二羟维生素D3, 抗炎, 缺血/再灌注, 小鼠

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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