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Ceftriaxone averts neuroinflammation and relieves depressive-like behaviors via GLT-1/TrkB signaling

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资源类型：
WOS体系：
Pubmed体系：

收录情况： ◇ SCIE

作者：
Gao Ruyan[1] * ; Ali Tahir[1] ; Liu Zizhen[1] ; Li Axiang[2] ; Hao Liangliang[3] ; He Liufang[4] ; Yu Xiaoming[5] ; Li Shupeng[1,6] ;
机构： [1]State Key Laboratory of Chemical Oncogenomics, Guangdong Provincial Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, Guangdong, 518055, People’s Republic of China [2]Institute of Forensic Injury, Institute of Forensic Bio-Evidence, Western China Science and Technology Innovation Harbor, Xi’an Jiaotong University, Xi’an, People’s Republic of China [3]Hospital of Chengdu, University of Traditional Chinese Medicine, No.39 Shi-er-qiao Road, Chengdu, People’s Republic of China [4]Department of Pediatrics, Shenzhen University General Hospital, Shenzhen University, People’s Republic of China [5]Cancer Center, The Second Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250033, People’s Republic of China [6]Institute of Chemical Biology, Shenzhen Bay Laboratory, People’s Republic of China
出处：
DOI： 10.1016/j.bbrc.2024.149550
ISSN：

关键词： Ceftriaxone LPS Neuroinflammation Depression GLT-1/TrkB

摘要：
The beneficial effect of a beta-lactam antibiotic, Ceftriaxone (CEF), to improve depressive-like symptoms has been documented previously, attributed to its modulation of glutamate neurotransmission. Here, we aimed to determine whether CEF could improve LPS-altered glutamatergic signaling associated with neuroinflammation-allied depression. To assess our goals, we established a neuroinflammation-allied depression mice model by injecting lipopolysaccharides (LPS), followed by behavioral and biochemical analysis. LPS-treated mice displayed depressive symptoms, neuroinflammation, dysregulated glutamate and its transporter (GLT-1) expression, altered expression of astrocyte reactive markers (GFAP, cxcl10, steap4, GBP2, and SRGN), and dysregulated BDNF/TrkB signaling. However, these changes were rescued by CEF treatment, as we found decreased neuroinflammation, relief of depression symptoms, and improved GLT-1 and BDNF/TrkB signaling upon CEF treatment. Moreover, GLT-1 and BDNF/TrkB regulation role of CEF was validated by K252a and DHK treatment. In summary, the anti-depressive effects of glutamate modulators, like CEF, are closely related to their anti-inflammatory role.Copyright © 2024. Published by Elsevier Inc.

基金：
Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions (2023SHIBS0004).
语种：
外文
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2023]版：
大类 | 3 区 生物学
小类 | 3 区 生物物理 4 区 生化与分子生物学
最新[2025]版：
大类 | 4 区 生物学
小类 | 4 区 生化与分子生物学 4 区 生物物理
JCR分区：
出版当年[2022]版：
Q2 BIOPHYSICS Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
最新[2023]版：
Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Q3 BIOPHYSICS

影响因子： 最新[2023版] 最新五年平均 出版当年[2022版] 出版当年五年平均 出版前一年[2021版] 出版后一年[2023版]

第一作者：
第一作者机构： [1]State Key Laboratory of Chemical Oncogenomics, Guangdong Provincial Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, Guangdong, 518055, People’s Republic of China
通讯作者：
通讯机构： [1]State Key Laboratory of Chemical Oncogenomics, Guangdong Provincial Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, Guangdong, 518055, People’s Republic of China [6]Institute of Chemical Biology, Shenzhen Bay Laboratory, People’s Republic of China
推荐引用方式(GB/T 7714)：
Gao Ruyan,Ali Tahir,Liu Zizhen,et al.Ceftriaxone averts neuroinflammation and relieves depressive-like behaviors via GLT-1/TrkB signaling[J].BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS.2024,701:149550.doi:10.1016/j.bbrc.2024.149550.
APA：
Gao Ruyan,Ali Tahir,Liu Zizhen,Li Axiang,Hao Liangliang...&Li Shupeng.(2024).Ceftriaxone averts neuroinflammation and relieves depressive-like behaviors via GLT-1/TrkB signaling.BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,701,
MLA：
Gao Ruyan,et al."Ceftriaxone averts neuroinflammation and relieves depressive-like behaviors via GLT-1/TrkB signaling".BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 701.(2024):149550

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