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醇通过调节NRF2/ARE/GSDMD信号通路来抑制缺血/再输液诱导的神经元亡

Feijian Zeng¹, Yao Liang², Yufei Wei¹

¹Section 2, Department of Encephalopathy, First Affiliated Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530023, China.

|August 23, 2025

概括

通过减少炎症和细胞死亡,保护脑细胞免受中风后的损伤. 它激活NRF2通路,有助于预防神经元亡,并可能为脑缺血/再输血损伤提供新的治疗方法.

科学领域:

神经科学
药理学
生物化学

背景情况:

醇 (CHR) 显示对缺血性中风 (IS) 的神经保护作用.
大脑缺血/再输损伤是中风相关的大脑损伤的重要原因.
了解CHR在I/R中的机制对于开发治疗策略至关重要.

研究的目的:

研究醇 (CHR) 对大脑缺血/再输血 (I/R) 损伤的保护作用.
在I/R模型中阐明CHR作用的基础分子机制.
评估CHR作为I/R损伤的治疗剂的潜力.

主要方法:

已建立的中脑动脉封闭/再输的小鼠模型 (MCAO/R) 和体外氧气-葡萄糖剥夺/再输 (OGD/R).
使用Nissl和TUNEL染色来评估神经损伤.
通过RT-qPCR,西部斑块,ELISA,CCK-8,LDH,流细胞计和光酶测试量基因表达,细胞因子释放和细胞功能.
研究了NRF2/ARE/GSDMD信号通路的作用.

主要成果:

在体内和体外I/ R模型中,CHR显著减轻了神经元损伤.
抑制了氧化应激,炎症和神经元灭.
CHR激活了NRF2/ARE信号通路,导致GSDMD的降低调节和减少热. 抑制NRF2导致神经元损伤.

结论:

醇 (CHR) 通过调节NRF2/ARE/GSDMD信号通路,对大脑I/R损伤进行神经保护.
CHR可以减少神经元的损失和烧死,突出其治疗潜力.
CHR是治疗大脑I/R损伤的一个有前途的治疗策略.

关键词:

大脑I/R损伤酸盐美国其他类型热症

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