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

IF 1.7 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL
Jialu Yu
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引用次数: 0

摘要

背景 神经细胞损伤是缺氧导致抑郁症状加重的一个重要原因,但其背后的机制尚不清楚。本研究旨在阐明过氧化物酶体增殖激活受体γ辅助激活因子1-α(PGC1α)/mitofusin-2(MFN2)信号轴在缺氧条件下小鼠抑郁症发病中的作用。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 + 高缺氧组(CUMS + H 组)。CUMS 组和 CUMS + H 组小鼠暴露于 CUMS 28 天。此外,CUMS + H 组的小鼠从第 21 天开始连续 7 天暴露于急性高氧环境。总共 28 天后,进行行为实验。所有小鼠均被麻醉并处死。分析了脑组织白细胞介素(IL)-6、活性氧(ROS)、三磷酸腺苷(ATP)和血清素(5-HT)的水平。结果 与CUMS组相比,CUMS + H组小鼠的IL-6和ROS水平升高,但开放场活动、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 急性高氧通过IL-6/PGC1α/MFN2信号通路在抑郁症的发病中发挥重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acute hyper-hypoxia accelerates the development of depression in mice via the IL-6/PGC1α/MFN2 signaling pathway
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.
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来源期刊
Open Medicine
Open Medicine Medicine-General Medicine
CiteScore
3.00
自引率
0.00%
发文量
153
审稿时长
20 weeks
期刊介绍: Open Medicine is an open access journal that provides users with free, instant, and continued access to all content worldwide. The primary goal of the journal has always been a focus on maintaining the high quality of its published content. Its mission is to facilitate the exchange of ideas between medical science researchers from different countries. Papers connected to all fields of medicine and public health are welcomed. Open Medicine accepts submissions of research articles, reviews, case reports, letters to editor and book reviews.
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