中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2017, Vol. 12 ›› Issue (3): 440-446.doi: 10.4103/1673-5374.202932

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

慢性冷暴露后海马的应激损伤和自噬变化

  

  • 收稿日期:2017-01-19 出版日期:2017-03-15 发布日期:2017-03-15
  • 基金资助:

    河南省重点高校教师基金（16A330001, 15A180031）；河南省博士后基金（2015051）；河南省基础与应用技术研究项目（162300410102）

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.

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摘要：

冷暴露作为一种外部的应激因素，不仅可造成皮肤冻伤，还能导致多种疾病的发生。作者既往研究表明，雌激素可能参与冷暴露后的神经保护，但具体机制尚不明确。为此，实验设计小鼠在10 oC环境暴露7d后，进一步在0–4 oC暴露30d，造成慢性冷暴露损伤模型。可见小鼠大脑海马CA1区氧化应激相关的c-fos和COX-2阳性表达的细胞增多，MAP1LC3标记的自噬细胞增多，Iba1标记的活化小胶质细胞增多，应激因子IL-1β阳性锥体细胞增多；实验结果还显示出慢性冷暴露显著提高了血液中雌激素及其受体GPR30水平。说明神经免疫反应参与了慢性冷暴露导致的海马氧化应激、神经细胞自噬和神经免疫反应方面的病理改变，而雌激素在冷暴露中发挥了神经保护效应。

ORCID:0000-0002-3323-7210(Lai Wang);0000-0002-3166-2686(Jin-bo Deng)

关键词: 神经再生, 慢性冷暴露, 氧化应激, 自噬, 小胶质细胞, 雌激素, 神经免疫, 海马CA1区

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