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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 &lt; 0.05), and in group C were still higher than those in group A (P &lt; 0.05). Arginase and CD206 were also detected in group A. they in group B were higher than those in group A (P &lt; 0.05), and in group C were even higher than those in group A (P &lt; 0.05). Immunofluorescence co-localization of CD45 and Arginase showed significantly increased fluorescence density at 6 h and 24 h after thermal injury (P &lt; 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.

Microglia Polarization in Heat-Induced Early Neural Injury