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急性高-低氧通过IL-6/PGC1α/MFN2信号通路加速小鼠抑郁症的发展。

Acute hyper-hypoxia accelerates the development of depression in mice via the IL-6/PGC1α/MFN2 signaling pathway.

作者信息

Yu Jialu

机构信息

Department of Anesthesiology, Guizhou Medical University, Guiyang, China.

Department of Clinical Medicine, Guizhou Medical University, 14 Beijing Road, Guiyang 550000, China.

出版信息

Open Med (Wars). 2024 Aug 9;19(1):20241001. doi: 10.1515/med-2024-1001. eCollection 2024.

DOI:10.1515/med-2024-1001
PMID:39135980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11317639/
Abstract

BACKGROUND

Neural cell damage is an important cause of exacerbation of depression symptoms caused by hypoxia, but the mechanism behind it is still unclear. The purpose of this study is to elucidate the role of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α)/mitofusin-2 (MFN2) signaling axis in the development of depression in mice under hypoxia.

METHODS

Male Institute of Cancer Research mice (age, 6 weeks) were assigned to the normal group, chronic unpredictable mild stress group (CUMS group), or CUMS + hyper-hypoxia group (CUMS + H group). Mice in the CUMS and CUMS + H groups were exposed to CUMS for 28 days. Additionally, mice in the CUMS + H group were exposed to acute hyper-hypoxia from Day 21 for 7 days. After a total of 28 days, behavioral experiments were conducted. All mice were anesthetized and sacrificed. Levels of brain tissue interleukin (IL)-6, reactive oxygen species (ROS), adenosine triphosphate (ATP), and serotonin (5-HT) were analyzed.

RESULTS

As compared to the CUMS group, mice in the CUMS + H group had increased IL-6 and ROS levels, but lower open-field activity, preference for sucrose, hippocampal neuronal membrane potential, ATP, and 5-HT levels, as well as MFN2 and PGC1α levels.

CONCLUSIONS

Acute hyper-hypoxia plays an important role in the development of depression via the IL-6/PGC1α/MFN2 signaling pathway.

摘要

背景

神经细胞损伤是缺氧导致抑郁症状加重的重要原因，但其背后的机制仍不清楚。本研究的目的是阐明过氧化物酶体增殖物激活受体γ共激活因子1α（PGC1α）/线粒体融合蛋白2（MFN2）信号轴在缺氧小鼠抑郁症发生发展中的作用。

方法

将雄性癌症研究所小鼠（6周龄）分为正常组、慢性不可预测轻度应激组（CUMS组）或CUMS + 高 - 低氧组（CUMS + H组）。CUMS组和CUMS + H组的小鼠接受28天的CUMS处理。此外，CUMS + H组的小鼠从第21天开始接受急性高 - 低氧处理，持续7天。共28天后，进行行为实验。所有小鼠麻醉后处死。分析脑组织白细胞介素（IL）-6、活性氧（ROS）、三磷酸腺苷（ATP）和血清素（5 - HT）水平。

结果

与CUMS组相比，CUMS + H组小鼠的IL - 6和ROS水平升高，但旷场活动、对蔗糖的偏好、海马神经元膜电位、ATP和5 - HT水平以及MFN2和PGC1α水平降低。

结论

急性高 - 低氧通过IL - 6/PGC1α/MFN2信号通路在抑郁症的发生发展中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/d715d9b692e7/j_med-2024-1001-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/bd1ac1e3e59c/j_med-2024-1001-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/b9e85f0c6114/j_med-2024-1001-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/441e2623f8c2/j_med-2024-1001-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/a8b74946e721/j_med-2024-1001-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/d715d9b692e7/j_med-2024-1001-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/bd1ac1e3e59c/j_med-2024-1001-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/b9e85f0c6114/j_med-2024-1001-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/441e2623f8c2/j_med-2024-1001-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/a8b74946e721/j_med-2024-1001-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5476/11317639/d715d9b692e7/j_med-2024-1001-fig005.jpg

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本文引用的文献

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