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高流动性组盒子1,一种新型的血清素受体-7负调节器,有助于M2微质铁和神经炎症在中风后抑郁症

Ou Du¹, Chao Wu², Yu-Xin Yang³

¹Department of Pharmacology, Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, West China School of Pharmacy, Sichuan University, Chengdu, Sichuan, China.

Free radical biology & medicine

|June 17, 2025

概括

高流动性组盒子1 (HMGB1) 负面调节血清素受体-7 (5-HT7R),通过促进微质铁和神经炎症,加剧中风后抑郁症. 抑制这种相互作用可能为中风恢复提供治疗效益.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

在中风后的神经炎症中,微质极化至关重要,其中涉及高流动性组盒1 (HMGB1) 和血清素受体-7 (5-HT7R).
在中风后抑郁症 (PSD) 的背景下,连接HMGB1和5-HT7R的精确机制仍然不完全理解.

研究的目的:

研究HMGB1和5-HT7R之间的相互作用及其在中风后抑郁症 (PSD) 中的作用.
阐明参与HMGB1诱导的微质激活和铁亡的分子通路.

主要方法:

生物发光共振能量转移 (BRET) 和共免疫沉 (Co-IP) 试验检查HMGB1-5-HT7R相互作用.
过渡性中脑动脉阻塞 (tMCAO) 鼠标模型用于研究体内效应.
对微质铁亡,神经炎症标志物以及cAMP/PKA和Nrf2/xCT/GPX4通路的分析.

主要成果:

HMGB1刺激上调的5-HT7R表达和下调的循环腺单酸盐 (cAMP) 积累.
在tMCAO模型中,5-HT7R删除或HMGB1抑制缓解了脑损伤,抑郁行为,M2微质铁亡和神经炎症.
HMGB1诱导的M2微质铁亡和神经炎症,抑制了cAMP/PKA和Nrf2/xCT/GPX4通路,效应因5-HT7R删除而减弱.

结论:

HMGB1作为5-HT7R的新型负调节剂,有助于缺血性脑损伤和PSD.
HMGB1-5-HT7R轴促进M2微质铁和神经炎症,为PSD提供潜在的治疗点.

关键词:

5-HT7RR是什么意思? 5-HT7R是什么意思?铁性化 (ferroptosis) 是一种这就是HMGB1的特点.神经炎症是一种神经炎症.脑卒中后的抑郁症是什么

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