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Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases.Estrogen might participate in neuroprotection after cold exposure,but its precise mechanism remains unclear.In this study,mice were exposed to 10°C for 7 days and 0–4°C for 30 days to induce a model of chronic cold exposure.Results showed that oxidative stress-related c-fos and cyclooxygenase 2 expressions,MAP1LC3-labeled autophagic cells,Iba1-labeled activated microglia,and interleukin-1β-positive pyramidal cells were increased in the hippocampal CA1 area.Chronic cold exposure markedly elevated the levels of estrogen in the blood and the estrogen receptor,G protein-coupled receptor 30.These results indicate that neuroimmunoreactivity is involved in chronic cold exposure-induced pathological alterations,including oxidative stress,neuronal autophagy,and neuroimmunoreactivity.Moreover,estrogen exerts a neuroprotective effect on cold exposure.
Cold exposure is an external stress factor that causes skin frostbite as well as a variety of diseases.Estrogen might participate in neuroprotection after cold exposure, but its precise mechanism remains unclear. In this study, mice were exposed to 10 ° C for 7 days and 0-4 ° C for 30 days to induce a model of chronic cold exposure. Results showed that oxidative stress-related c-fos and cyclooxygenase 2 expressions, MAP1LC3-labeled autophagic cells, Iba1-labeled activated microglia, and interleukin-1β-positive Chronic cold exposure markedly elevated the levels of estrogen in the blood and the estrogen receptor, G protein-coupled receptor 30. These results that that neuroimmunoreactivity is involved in chronic cold exposure-induced pathological alterations, including oxidative stress, neuronal autophagy, and neuroimmunoreactivity. Moreover, estrogen exerts a neuroprotective effect on cold exposure.