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给小鼠补充分子氢可改善脂多糖诱导的兴趣丧失。

Molecular hydrogen supplementation in mice ameliorates lipopolysaccharide-induced loss of interest.

作者信息

Koga Minori, Sato Mayumi, Nakagawa Ryuichi, Tokuno Shinichi, Asai Fumiho, Maezawa Yuri, Nagamine Masanori, Yoshino Aihide, Toda Hiroyuki

机构信息

Department of Psychiatry, School of Medicine National Defense Medical College Saitama Japan.

Graduate School of Health Innovation Kanagawa University of Human Services Kanagawa Japan.

出版信息

PCN Rep. 2024 Aug 21;3(3):e70000. doi: 10.1002/pcn5.70000. eCollection 2024 Sep.

DOI:10.1002/pcn5.70000
PMID:39171191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11337204/
Abstract

AIM

The objective of this study was to evaluate the potential of hydrogen in preventing and treating psychiatric symptoms, particularly depressed mood and loss of interest, and to explore its underlying mechanisms. A mouse model exhibiting inflammation-derived depressive symptoms was used for the investigation.

METHODS

Institute of Cancer Research mice were subjected to a 7-day intervention of either 30% hydrogen or 40 g per day of air via jelly intake. On the final day, lipopolysaccharide (LPS) was intraperitoneally administered at 5 mg/kg to induce inflammation-related depressive symptoms. Behavioral and biochemical assessments were conducted 24 h post-LPS administration.

RESULTS

Following LPS administration, a decrease in spontaneous behavior was observed; however, this effect was mitigated in the group treated with hydrogen. The social interaction test revealed a significant reduction in interactions with unfamiliar mice in the LPS-treated group, whereas the hydrogen-treated group exhibited no such decrease. No significant changes were noted in the forced-swim test for either group. Additionally, the administration of LPS in the hydrogen group did not result in a decrease in zonula occludens-1, a biochemical marker associated with barrier function at the cerebrovascular barrier and expressed in tight junctions.

CONCLUSION

Hydrogen administration demonstrated a preventive effect against the LPS-induced loss of interest, suggesting a potential role in symptom prevention. However, it did not exhibit a suppressive effect on depressive symptoms in this particular model. These findings highlight the nuanced impact of hydrogen in the context of inflammation-induced psychiatric symptoms, indicating potential avenues for further exploration and research.

摘要

目的

本研究的目的是评估氢气在预防和治疗精神症状,特别是情绪低落和兴趣丧失方面的潜力,并探讨其潜在机制。使用表现出炎症性抑郁症状的小鼠模型进行研究。

方法

将癌症研究所的小鼠通过摄入果冻接受为期7天的30%氢气或每天40克空气的干预。在最后一天,以5毫克/千克的剂量腹腔注射脂多糖(LPS)以诱导炎症相关的抑郁症状。在注射LPS后24小时进行行为和生化评估。

结果

注射LPS后,观察到自发行为减少;然而,在氢气处理组中这种效应得到缓解。社交互动测试显示,LPS处理组与陌生小鼠的互动显著减少,而氢气处理组没有出现这种减少。两组在强迫游泳测试中均未观察到显著变化。此外,在氢气组中注射LPS并未导致紧密连接蛋白-1减少,紧密连接蛋白-1是一种与脑血管屏障的屏障功能相关且在紧密连接中表达的生化标志物。

结论

氢气给药对LPS诱导的兴趣丧失具有预防作用,表明其在症状预防方面具有潜在作用。然而,在这个特定模型中,它对抑郁症状没有抑制作用。这些发现突出了氢气在炎症诱导的精神症状背景下的细微影响,为进一步探索和研究指明了潜在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/423d71fe59ad/PCN5-3-e70000-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/69eac5735508/PCN5-3-e70000-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/809552e4e583/PCN5-3-e70000-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/8614a8dedd1a/PCN5-3-e70000-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/95cb00a44aab/PCN5-3-e70000-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/d7ad3ff26654/PCN5-3-e70000-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/d4e182627a79/PCN5-3-e70000-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/91a32bd8bc49/PCN5-3-e70000-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/423d71fe59ad/PCN5-3-e70000-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/69eac5735508/PCN5-3-e70000-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/809552e4e583/PCN5-3-e70000-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/8614a8dedd1a/PCN5-3-e70000-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/95cb00a44aab/PCN5-3-e70000-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/d7ad3ff26654/PCN5-3-e70000-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/d4e182627a79/PCN5-3-e70000-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/91a32bd8bc49/PCN5-3-e70000-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/447e/11337204/423d71fe59ad/PCN5-3-e70000-g005.jpg

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