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运动过程中小鼠海马体的信使核糖核酸表达谱及生物信息学分析:通过海马体信使核糖核酸谱变化减轻甲基苯丙胺依赖

Messenger RNA expression profiles and bioinformatics analysis of mouse hippocampi during exercise alleviates methamphetamine dependence via mRNA profile change in hippocampi.

作者信息

Li Yue, Re Guo-Fen, Zhao Yu, Kong Deshenyue, Mao Jun-Hong, Wang Kun-Hua, Kuang Yi-Qun

机构信息

NHC Key Laboratory of Drug Addiction Medicine, First Affiliated Hospital of Kunming Medical University, Kunming Medical University, Kunming, China.

Scientific Research Laboratory Center, First Affiliated Hospital of Kunming Medical University, Kunming, China.

出版信息

Ann Transl Med. 2022 Sep;10(18):957. doi: 10.21037/atm-22-450.

DOI:10.21037/atm-22-450
PMID:36267776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9577721/
Abstract

BACKGROUND

Methamphetamine (METH) is a highly addictive, psychoactive drug which can harm individual health and lead to great social problems. Various approaches have been adopted to address the problems arising from METH addiction, but relapse rates remain high. Recently, it has been found that comprehensive treatment combined with scientific and appropriate exercise interventions can improve the mental state and physical fitness of drug addicts and promote their physical and mental rehabilitation. Long-term, regular exercise improves the symptoms of METH withdrawal and reduces METH relapse. This study aimed to investigate the effects and regulated gene expression related to running exercise in METH-addicted mice.

METHODS

Male C57BL/6J mice were used to construct a METH addiction model. We performed a running exercise intervention and used conditioned place preference (CPP) to measure the effects of the running intervention on the METH-addicted mice. We also performed RNA sequencing (RNA-seq) and transcriptome analysis on the mice hippocampi, and the functions and differentially expressed genes (DEGs) that were significantly regulated by exercise intervention in the METH-addicted mice were analyzed and noted.

RESULTS

The results showed that days of CPP were shortened to 3 days in METH-addicted mice that underwent moderate exercise intervention, compared to 6 days in METH-addicted mice that went without exercise intervention. In addition, hippocampal transcriptome analysis revealed 12 DEGs significantly regulated by exercise intervention. By performing Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, it was revealed that the function of immune responses was significantly enriched in the METH-addicted mice undertaking exercise. The expression of 12 DEGs was verified by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR), which showed that relative messenger RNA (mRNA) expression of DEGs was consistent with the RNA-seq results.

CONCLUSIONS

A running intervention can promote the recovery of METH addiction in mice, and the 12 candidate DEGs from the mouse hippocampus can be used for further research on the regulatory mechanisms of exercise in METH-addicted mice.

摘要

背景

甲基苯丙胺(METH)是一种极易成瘾的精神活性药物,会损害个人健康并引发严重的社会问题。人们已采取多种方法来解决甲基苯丙胺成瘾引发的问题,但复发率仍然很高。最近发现,综合治疗结合科学适当的运动干预可以改善吸毒者的精神状态和身体素质,促进其身心康复。长期、规律的运动可改善甲基苯丙胺戒断症状并减少甲基苯丙胺复发。本研究旨在探讨跑步运动对甲基苯丙胺成瘾小鼠的影响及相关基因表达的调控情况。

方法

使用雄性C57BL/6J小鼠构建甲基苯丙胺成瘾模型。我们进行了跑步运动干预,并使用条件性位置偏爱(CPP)来测量跑步干预对甲基苯丙胺成瘾小鼠的影响。我们还对小鼠海马体进行了RNA测序(RNA-seq)和转录组分析,并分析记录了运动干预在甲基苯丙胺成瘾小鼠中显著调控的功能和差异表达基因(DEG)。

结果

结果显示,接受适度运动干预的甲基苯丙胺成瘾小鼠的CPP天数缩短至3天,而未接受运动干预的甲基苯丙胺成瘾小鼠的CPP天数为6天。此外,海马体转录组分析显示有12个DEG受运动干预显著调控。通过进行基因本体论(GO)和京都基因与基因组百科全书(KEGG)通路富集分析,发现在进行运动的甲基苯丙胺成瘾小鼠中免疫反应功能显著富集。通过实时定量逆转录聚合酶链反应(qRT-PCR)验证了12个DEG的表达,结果表明DEG的相对信使核糖核酸(mRNA)表达与RNA-seq结果一致。

结论

跑步干预可促进小鼠甲基苯丙胺成瘾的恢复,从小鼠海马体中筛选出的12个候选DEG可用于进一步研究运动对甲基苯丙胺成瘾小鼠的调控机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/0721aa77df14/atm-10-18-957-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/303551e9d9cd/atm-10-18-957-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/91ae882c04ca/atm-10-18-957-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/c2828dbb39e3/atm-10-18-957-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/4be82fcca045/atm-10-18-957-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/ac4bd2362bc4/atm-10-18-957-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/0721aa77df14/atm-10-18-957-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/303551e9d9cd/atm-10-18-957-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/91ae882c04ca/atm-10-18-957-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/c2828dbb39e3/atm-10-18-957-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/4be82fcca045/atm-10-18-957-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/ac4bd2362bc4/atm-10-18-957-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f567/9577721/0721aa77df14/atm-10-18-957-f6.jpg

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