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USP25通过降低TAB2的含量来抑制脑性缺血性中风后的神经炎症反应

Zhongding Li^1,2, Baohua Liu², Kate Lykke Lambertsen^3,4,5

¹Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine, Vision and Brain Health), School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|August 17, 2023

概括

乌比基特异性蛋白酶USP25的缺乏会使缺血性中风损伤恶化. USP25通过调节TAB2来抑制微质驱动的神经炎症,这表明USP25是中风的潜在治疗点.

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:

大脑缺血性中风是一个主要的全球健康问题,伤害机制尚不清楚.
确定新的治疗点对于减轻中风相关的发病率和死亡率至关重要.

研究的目的:

为了研究在缺血性中风损伤的背景下,乌比奎丁特异性蛋白酶USP25的作用.
阐明USP25影响中风病理学的潜在分子机制.

主要方法:

利用小鼠缺血性中风模型来评估USP25缺乏的影响.
研究了USP25对神经元死亡,神经炎症和特定信号通路 (NF-κB,MAPK) 的影响.
采用AAV9介导的基因敲除来验证TAB2.2的作用.

主要成果:

USP25缺乏在小鼠中显著加重缺血性中风损伤.
USP25抑制了微质介导的神经炎症,减少了神经元损失和神经学缺陷.
USP25二基因化TAB2,限制NF-κB和MAPK的信号激活.
TAB2的倒置改善了中风损伤,证实了它在USP25的保护作用中的作用.
USP25在老鼠和人类大脑的缺血半阴层内的微质上调.

结论:

USP25作为缺血性中风损伤的关键抑制剂.
USP25通过TAB2通路调节微质激活和神经炎症来发挥其保护作用.
USP25代表了治疗缺血性中风的有前途的治疗标.

关键词:

美国25美大脑缺血性中风是脑中风.微质细胞中的微质细胞神经炎症是一种神经炎症.无处不在的化

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