Aquaporin-1 regulates microglial polarization and inflammatory response in traumatic brain injury

被引：0

作者：

Ma, Yixuan ^{[1
]}

Huang, Yimin ^{[1
]}

Liu, Xuyang ^{[1
]}

Jiao, Liwu ^{[1
]}

Zhu, Hongtao ^{[1
]}

Chen, Zhiye ^{[1
]}

Wu, Zhuojin ^{[1
]}

Shen, Yuanzhong ^{[1
]}

Lin, Kehan ^{[1
]}

Hu, Feng ^{[1
]}

Shu, Kai ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Neurosurg, 1095 Jiefang Ave, Wuhan 430030, Hubei, Peoples R China

来源：

INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE | 2025年 / 55卷 / 03期

关键词：

TBI; microglia; AQP1; inflammation; RECOVERY;

D O I：

10.3892/ijmm.2025.5482

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The present study investigated the mechanisms by which aquaporin 1 (AQP1) influences microglial polarization and neuroinflammatory processes in traumatic brain injury (TBI). A model of TBI was generated in AQP1-knockout mice to assess the impact of AQP1 deletion on inflammatory cytokine release, neuronal damage and cognitive function. Immunofluorescence, reverse transcription-quantitative PCR, western blotting and enzyme-linked immunosorbent assay were employed to evaluate pro-inflammatory and anti-inflammatory markers. Behavioral assessments, including the Barnes maze, were performed to determine cognitive outcomes. Moreover, AQP1 knockout inhibited the activation of inflammation-related signaling pathways, including nuclear factor-kappa B, Janus kinase/signal transducer and activator of transcription, phosphoinositide 3-kinase/protein kinase B and extracellular signal-regulated kinase/mitogen-activated protein kinase pathways. Further studies indicated that the AQP1 inhibitor m-phenylenediacrylic acid demonstrated significant neuroprotective effects in a mouse model of TBI. These findings suggested that AQP1 may be essential in post-TBI inflammatory responses and neuronal injury, establishing a theoretical foundation for future therapies aimed at AQP1.

引用

页数：14

共 39 条

[1]

American Veterinary Medical Association, 2020, AVMA guidelines for the euthanasia of animals

[2] Traumatic Brain Injury Induces cGAS Activation and Type I Interferon Signaling in Aged Mice [J].