电磁辐射（EMF）具有中枢神经损伤效应，但机理不明，且难于有效防护。我们前期研究发现：热习服可减轻EMF中枢神经损伤效应，并可能与其调节小胶质细胞M2型活化有关。由于热习服可诱导大量HSP60产生，而HSP60又是调节小胶质细胞活化关键分子TREM2的配体。据此我们推测：热习服可能通过HSP60/TREM2及其信号通路调节小胶质细胞M2型活化，从而对EMF导致的中枢损伤产生保护作用。为进一步验证假设并探讨机理，本项目主要研究①热习服调节EMF刺激的小胶质细胞M2型活化与中枢神经保护作用之间的相关性；②HSP60、TREM2作为触发分子在热习服调节EMF刺激的小胶质细胞M2型活化中的关键作用；③HSP60/TREM2下游信号通路PI3K/Akt调节小胶质细胞M2型活化的机制。本项目不仅可揭示热习服对EMF中枢神经损伤保护作用的机制，而且有望为EMF暴露职业人群提供一条切实可行的有效防护措施。

It has been reported that the electromagnetic fields(EMF) exposure could initiate the central neverous system(CNS) injury. But the machanism is not so clear and it is hard to prevent.In the three previous research projects supported by NSCF, we have proved that EMF stimulate M1 phenotype activation of microglia, which contributed to the CNS injury induced by EMF exposure. Our recently studies found that heat acclimation attenuates CNS injury, improve the functional recovery and modulate microglial M2 phenotype activation after EMF exposure. It has been proved that heat acclimation induce high expression of Hsp60. Moreover,Hsp60 is a ligand of TREM2 which is the key receptor trigger microglia activation. Based on these research results, we hypothesis that heat acclimation protect CNS against EMF exposure through modulate microglia M2 phenotype activation, which is switched on by HSP60/TREM2. We plan to study: (1)The relationship between activation and the neuroprotection induced by heat acclimation after EMF exposure. (2)The role of HSP60、TREM2 as the gateway in heat acclimation modulating the M2 phenotype activation of microglia stimulated by EMF. (3) The mechanism of PI3K/Akt signal transduction transer the signal of HSP60/TREM2 and regulate microglial M2 phenotype activation. This study could explore the cellular and molecular mechanism of the neuroprotect in heat acclimation attenuates CNS injury induced by EMF exposure, and provide a effective and feasible method to protect occupational population against EMF injury.