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

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.

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).

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.