NEUROSURGERY / RESEARCH PAPER
Microglia Polarization in Heat-Induced Early Neural Injury
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1
Department of Emergency Center, Affiliated Hospital 2 of Nantong University, Nantong, Jiangsu, China;
2
Department of Dermatology, Affiliated Hospital 3 of Nantong University,Nantong, Jiangsu, 226001, China
3
Department of Neurosurgery, Affiliated Hospital 2 of Nantong University, Nantong, Jiangsu, China
CORRESPONDING AUTHOR
lei wang   

Department of Emergency Center, Affiliated Hospital 2 of Nantong University, Nantong, Jiangsu, China;
Submission date: 2019-09-23
Final revision date: 2019-12-31
Acceptance date: 2020-01-12
Online publication date: 2021-03-25
 
 
KEYWORDS
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ABSTRACT
Introduction:
observe the polarization of microglia in response to heat-induced early nerve injury and to explore its possible mechanism of action.

Material and methods:
18 dogs were divided into control (group A) and experimental groups (group B, C and D) ,Western blot analysis was used to detect the expression of microglia-specific markers CD45, iNOS, Arginase, and CD206 in normal and heat-damaged brain tissues at different time points (1 h, 6 h, 24 h).

Results:
CD45 and iNOS were detected in group A. The two protein markers in group B were significantly higher than those in group A (P < 0.05), and in group C were still higher than those in group A (P < 0.05). Arginase and CD206 were also detected in group A. they in group B were higher than those in group A (P < 0.05), and in group C were even 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).

Conclusions:
After heat-induced disease, microglia were found active in the brain tissues of dogs. The microglia activated in the early 1-6 h of central nervous system injury were mainly the M1 type, which were then converted to the M2 type after 6 h. The 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 understanding central nervous system injury in heat-induced disease.

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ISSN:1734-1922