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中华神经创伤外科电子杂志 ›› 2019, Vol. 05 ›› Issue (05) : 299 -303. doi: 10.3877/cma.j.issn.2095-9141.2019.05.010

所属专题: 文献

基础研究

小胶质细胞极化在热损伤介导的早期神经损伤中的相关研究
王蕾1, 叶子2, 张毅2, 朱保锋1, 沈一鸣1, 储鑫1, 戴勇2, 沈君华1,()   
  1. 1. 226001 南通,南通大学第二附属医院急诊中心
    2. 226001 南通,南通大学第二附属医院神经外科
  • 收稿日期:2019-07-02 出版日期:2019-10-15
  • 通信作者: 沈君华
  • 基金资助:
    江苏省科技厅自然科学基金(BK20161290); 南通市科技计划项目(JCZ18004,JC2018088); 江苏省"六大人才高峰"高层次人才项目(2019-WSW-199)

Study on microglia polarization in early neural injury mediated by thermal injury

Lei Wang1, Zi Ye2, Yi Zhang2, Baofeng Zhu1, Yiming Shen1, Xin Chu1, Yong Dai2, Junhua Shen1,()   

  1. 1. Department of Emergency Center, Second Affiliated Hospital of Nantong University, Nantong 226001, China
    2. Department of Neurosurgery, Second Affiliated Hospital of Nantong University, Nantong 226001, China
  • Received:2019-07-02 Published:2019-10-15
  • Corresponding author: Junhua Shen
  • About author:
    Corresponding author: Shen Junhua, Email:
引用本文:

王蕾, 叶子, 张毅, 朱保锋, 沈一鸣, 储鑫, 戴勇, 沈君华. 小胶质细胞极化在热损伤介导的早期神经损伤中的相关研究[J/OL]. 中华神经创伤外科电子杂志, 2019, 05(05): 299-303.

Lei Wang, Zi Ye, Yi Zhang, Baofeng Zhu, Yiming Shen, Xin Chu, Yong Dai, Junhua Shen. Study on microglia polarization in early neural injury mediated by thermal injury[J/OL]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2019, 05(05): 299-303.

目的

观察小胶质细胞在热损伤介导的早期神经损伤中的极化状态并探讨其可能机制。

方法

通过建立Beagle犬热射病动物模型,按随机数字表法将18只Beagle犬分为正常对照组(A组)9只,根据热损伤后不同时间点(1、6、24 h)分为B、C、D组各3只,B~D组置于动物体温维持仪的电热毯上,温度设置为40℃±0.5℃,每5 min监测1次直肠温度直至达到40℃。建模成功后转移到26℃±0.5℃温度和60%±0.5%湿度的环境。4组18只Beagle犬均取下丘脑进行Western blot检测,检测小胶质细胞特异性标志物CD45、iNOS及Arginase、CD206分别在4组小胶质细胞中的表达。进一步免疫组织荧光共定位观察CD45、Arginase表达。

结果

A组检测出少许CD45及iNOS蛋白,B、C组两种蛋白标志物均显著高于A组(P<0.05),而D组较A组差异无统计学意义(P>0.05);A组检测出少许Arginase及CD206蛋白,B、C、D组两种蛋白标志物均高于A组,差异有统计学意义(P<0.05)。免疫组织荧光共定位CD45、Arginase,分别在热损伤后6 h和24 h荧光光密度显著增强,差异有统计学意义(P<0.001)。

结论

热射病后Beagle犬脑组织可见小胶质细胞极化活跃,中枢神经系统损伤早期1~6 h小胶质细胞活化主要以M1型为主,6 h后则转化为M2为主,热射病后24 h M2型占优势。M1/M2极化趋势与热射病早期脑损伤的相互关系可能成为热射病中枢神经损伤关键。

Objective

To observe the polarization of microglia in early nerve injury mediated by thermal injury and investigate its possible mechanism.

Methods

Eighteen Beagle dogs were divided into control group (group A, n=9) according to the random number table method by establishing a Beagle dog heatstroke animal model. According to different time points after heat injury (1, 6, 24 h), the dogs were divided into group B, C, D with 3 dogs each. The experimental group were placed on the electric blanket of the animal temperature maintenance instrument; the temperature was set to 40℃±0.5℃, and the rectal temperature was monitored every 5 min until reaching 40℃. After successful modeling, transfer them to an environment of 26℃±0.5℃ temperature and 60%±0.5% humidity. Hypothalami were taken out from four groups of 18 Beagle dogs, and were subjected to Western blot analysis to detect the expression of microglia-specific markers CD45, iNOS, Arginase and CD206 in 4 groups of microglia. Further immunohistochemical fluorescence co-localization was used to observe the expression of CD45 and Arginase.

Results

A little CD45 and iNOS protein were detected in group A. The two protein markers in group B and C were significantly higher than those in group A (P<0.05). There was no statistically significant difference between the group D and group A (P>0.05). A little Arginase and CD206 protein were also detected in group A. The two protein markers in group B, C, D were higher than those in group A (P<0.05). Immunofluorescence co-localization of CD45 and Arginase showed significantly increased fluorescence density at 6 h and 24 h after thermal injury (P<0.001).

Conclusion

After heat stroke, microglia were active in the brain tissue of Beagle dogs. The microglia activated in the early 1-6 h of central nervous system injury was mainly the M1 type, which then converted to M2 type after 6 h. After 24 h M2 type was dominant. The relationship between M1/M2 polarization trends and early brain injury in heat-induced disease may be a key to central nervous system injury in heat-induced disease.

图1 4组热损伤后小胶质细胞M1/M2蛋白表达
图2 免疫组织荧光共定位M1/M2型标志物表达
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