| 注册
首页|期刊导航|中国实验动物学报|阿格拉宾通过抑制NLRP3炎症小体活化调控创伤性脑损伤小鼠神经炎症

阿格拉宾通过抑制NLRP3炎症小体活化调控创伤性脑损伤小鼠神经炎症

方壹万 周诗雨 姬浩鑫 闫华筝 高建雄 李睦融 吕合作 周慧芳

中国实验动物学报2025,Vol.33Issue(12):1715-1726,12.
中国实验动物学报2025,Vol.33Issue(12):1715-1726,12.DOI:10.3969/j.issn.1005-4847.2025.12.001

阿格拉宾通过抑制NLRP3炎症小体活化调控创伤性脑损伤小鼠神经炎症

Arglabin regulates neuroinflammation in mice with traumatic brain injury by inhibiting NLRP3 inflammasome activation

方壹万 1周诗雨 2姬浩鑫 2闫华筝 2高建雄 2李睦融 3吕合作 2周慧芳4

作者信息

  • 1. 蚌埠医科大学EYE-X研究院,安徽 蚌埠 233030||蚌埠医科大学慢性疾病免疫学基础与临床安徽省重点实验室,安徽 蚌埠 233030
  • 2. 蚌埠医科大学慢性疾病免疫学基础与临床安徽省重点实验室,安徽 蚌埠 233030
  • 3. 蚌埠医科大学检验医学院,安徽 蚌埠 233030
  • 4. 蚌埠医科大学EYE-X研究院,安徽 蚌埠 233030
  • 折叠

摘要

Abstract

Objective To explore the effects and mechanism of arglabin on neuroinflammation in mice with traumatic brain injury(TBI).Methods Adult male C57BL/6J mice were divided randomly into:sham operation(Sham),Sham+Arglabin,TBI and TBI+Arglabin groups.TBI was induced by controlled cortical impact.After successful modeling,mice received 5 μg/kg arglabin by intraperitoneal injection,once a day until the material was retrieved.Neurological function was evaluated 3 weeks after the operation.Hematoxylin-eosin(HE)and Nissl staining were performed 4 weeks after the operation.Relative protein expression levels of NLRP3,apoptosis-associated speck-like protein containing a caspase-recruitment domain(ASC),and Caspase-1 in brain tissues were detected by Western Blot 3 d after surgery,and relative mRNA levels of the inflammatory factors interleukin(IL)-1β,IL-18,IL-6,inducible nitric oxide synthase(iNOS),IL-4,and Arg1 were detected by RT-qPCR.M1 and M2 cells were observed 7 d after the operation.Results Compared with the findings in the Sham group,in TBI group mice,nerve function was reduced(P<0.0001),the brain-tissue damage area was significantly increased(P<0.01),and neurons were largely lost(P<0.01).Additionally,NLRP3,ASC,and Caspase-1 protein levels in brain tissue were significantly increased(P<0.05),the proinflammatory cytokines IL-1β,IL-18,IL-6,and iNOS were significantly increased(P<0.05),and the anti-inflammatory cytokines IL-4 and Arg1 were significantly decreased(P<0.01).Lastly,levels of M1 type cells were significantly increased(P<0.01).Compared with the findings in the TBI group,in the TBI+Arglabin group,nerve function was significantly improved(P<0.01),the brain tissue-damage area was significantly reduced(P<0.01),neuronal loss was significantly reduced(P<0.01),In addition,NLRP3,ASC,and Caspase-1 proteins in brain tissue were significantly reduced(P<0.05),the proinflammatory cytokines IL-1β,IL-18,IL-6,and iNOS were significantly reduced(P<0.05),the anti-inflammatory cytokines IL-4 and Arg1 were significantly increased(P<0.01),and M2 type cells were significantly increased(P<0.01).Conclusions Arglabin improves the local immune microenvironment by inhibiting NLRP3 inflammasome activation to alleviate neuroinflammation in mice with TBI.

关键词

创伤性脑损伤/神经炎症/阿格拉宾/NLRP3炎症小体

Key words

traumatic brain injury/neuroinflammatory/Arglabin/NLRP3 inflammasome

分类

生物科学

引用本文复制引用

方壹万,周诗雨,姬浩鑫,闫华筝,高建雄,李睦融,吕合作,周慧芳..阿格拉宾通过抑制NLRP3炎症小体活化调控创伤性脑损伤小鼠神经炎症[J].中国实验动物学报,2025,33(12):1715-1726,12.

基金项目

国家自然科学基金(82072416),蚌埠医科大学第一附属医院高水平科技创新团队资助项目(BYYFY2022TD001),国家级大学生创新训练项目(202410367086). Funded by National Natural Science Foundation of China(82072416),High-Level Science and Technology Innovation Team Funded by the First Affiliated Hospital of Bengbu Medical University(BYYFY2022TD001),National College Student Innovation Training Project(202410367086). (82072416)

中国实验动物学报

OA北大核心

1005-4847

访问量0
|
下载量0
段落导航相关论文