Neural Regeneration Research ›› 2017, Vol. 12 ›› Issue (3): 440-446.doi: 10.4103/1673-5374.202932

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Stress injuries and autophagy in mouse hippocampus after chronic cold exposure

Ting-ting Qu1, 2, Jie-xin Deng1 , Rui-ling Li1, Zhan-jun Cui1, Xiao-qing Wang1, Lai Wang1, Jin-bo Deng1   

  1. 1 Institute of Neurobiology, College of Life Science, Henan University, Kaifeng, Henan Province, China; 2 Nursing College, Henan Vocational College of Applied Technology, Zhengzhou, Henan Province, China
  • Received:2017-01-19 Online:2017-03-15 Published:2017-03-15
  • Contact: Lai Wang, M.D. or Jin-bo Deng, M.D., wanglai@henu.edu.cn or jinbo_deng@henu.edu.cn.
  • Supported by:

    This study was supported by the Henan Province Foundation for Key University Teachers in China, No. 16A330001, 15A180031; the Henan Postdoctoral Foundation in China, No. 2015051; a grant from the Henan Province Research Program of Basic and Advanced Technology
    in China, No. 162300410102.

Abstract:

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.

Key words: nerve regeneration, chronic cold exposure, oxidative stress, autophagy, microglial cells, neuroimmunoreactivity, hippocampal CA1 area, estrogen, neural regeneration