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大麻二酚激活Nrf2-Keap1信号通路抑制TBI大鼠氧化应激反应

ZHU Juan LI Ping LI Hengxi LI Jiali LING Tenghan CAO Yan YIN Aiping MA Yuan GUO Xiaobing WU Haiying

中国免疫学杂志2025,Vol.41Issue(12):2824-2830,7.
中国免疫学杂志2025,Vol.41Issue(12):2824-2830,7.DOI:10.3969/j.issn.1000-484X.2025.12.002

大麻二酚激活Nrf2-Keap1信号通路抑制TBI大鼠氧化应激反应

Cannabidiol activates Nrf2-Keap1 signaling pathway to inhibit oxidative stress in TBI rats

ZHU Juan 1LI Ping 1LI Hengxi 1LI Jiali 1LING Tenghan 1CAO Yan 1YIN Aiping 1MA Yuan 1GUO Xiaobing 1WU Haiying2

作者信息

  • 1. Department of Human Anatomy&Embryology,School of Basic Medicine,Kunming Medical University,Kunming 650500,China
  • 2. Department of Emergency and Intensive Care Unit,the First Affiliated Hospital of Kunming Medical University,Kunming 650032,China
  • 折叠

摘要

Abstract

Objective:To investigate the protective effect of cannabidiol(CBD)against oxidative stress in rats with traumatic brain injury(TBI)and its relationship with Nrf2-Keap1 signaling pathway.Methods:Adult male SD rats were randomly divided into sham-operated group(Sham),model group(TBI+vehicle),CBD-intervention group(TBI+CBD)and pathway inhibitor group(TBI+CBD+ML385).Modified Feeney free-fall method was used to establish TBI model rats,pathological changes,oxidative stress and inflammation in rat brain tissue were observed by combination of neurological deficit scoring(mNSS),HE staining,immunofluores-cence staining,Western blot,RT-qPCR and ELISA.Results:mNSS score was significantly increased and pathological changes such as abnormal neuronal cell morphology and inflammatory cell infiltration were observed in model group,IL-1β and TNF-α positive expressions were significantly enhanced,GSH content and Nrf2 protein expression were significantly reduced,ROS,MDA contents and Keap1 mRNA were significantly increased.mNSS score was significantly reduced in TBI+CBD group,pathological condition of brain tissue was improved,IL-1β,TNF-α positive expressions were reduced,GSH content and Nrf2 expression were significantly increased,ROS,MDA contents and Keap1 mRNA were significantly decreased,and ML385 could significantly inhibit antioxidant effect of CBD.Conclusion:CBD can inhibit oxidative stress after TBI through Nrf2-Keap1 pathway,reduce secondary pathological injury in TBI rats,and play a certain neuroprotective role.

关键词

创伤性脑损伤/大麻二酚/氧化应激/Nrf2-Keap1信号通路

Key words

Traumatic brain injury/Cannabidiol/Oxidative stress/Nrf2-Keap1 signaling pathway

分类

医药卫生

引用本文复制引用

ZHU Juan,LI Ping,LI Hengxi,LI Jiali,LING Tenghan,CAO Yan,YIN Aiping,MA Yuan,GUO Xiaobing,WU Haiying..大麻二酚激活Nrf2-Keap1信号通路抑制TBI大鼠氧化应激反应[J].中国免疫学杂志,2025,41(12):2824-2830,7.

基金项目

国家自然科学基金地区科学基金(82060241,82260387,82560263) (82060241,82260387,82560263)

云南省基础研究计划项目-重点项目(202501AS070026) (202501AS070026)

云南省教育厅科学研究基金(2023J0217) (2023J0217)

云南省科技厅科技计划基础研究专项(202301AS070020) (202301AS070020)

云南省科技厅昆明医科大学应用基础研究联合专项(202101AY070001-037) (202101AY070001-037)

国家大学生创新训练项目(202210678029). (202210678029)

中国免疫学杂志

OA北大核心

1000-484X

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