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长非编码RNA 1810026B05Rik通过NF-κB通路激活调解大脑缺血症/再输液诱导的神经损伤

Hao Zhang¹, Meng Li¹, Jiayu Yao²

¹Institute of Biomedical and Pharmaceutical Sciences, Guangdong University of Technology, Guangzhou 510006, China.

International journal of molecular sciences

|October 16, 2025

概括

研究人员确定了一种新型长非编码RNA,CHASERR (lncRNA-1810026B05Rik),通过激活NF-κB通路,在脑缺血/再损伤中加剧神经炎症和神经元亡. 降低CHASERR的调节显示出对中风的保护作用,这表明它是治疗点.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

大脑缺血/反 (I/R) 损伤导致神经炎症和亡导致显著的神经损伤.
长非编码RNAs (lncRNAs) 涉及各种生物过程,但它们在大脑I / R损伤中的作用尚未完全理解.

研究的目的:

为了识别涉及大脑I/R损伤的新型 lncRNA.
阐明已识别的lncRNAs调节I/R损伤中的神经炎症和亡的分子机制.
评估针对这些lncRNA用于中风治疗的治疗潜力.

主要方法:

在鼠模型中进行的转录学分析,用于对焦大脑I/R.
在小鼠MCAO/R和老鼠OGD/R模型中分析lncRNA表达.
研究了lncRNA-1810026B05Rik (CHASERR) 和IκBα之间的相互作用.
评估CHASERR对NF-κB通路激活和神经元亡的影响.

主要成果:

在脑I/R损伤模型中, lncRNA-1810026B05Rik (CHASERR) 表达是上调调的.
CHASERR在物理上与IκBα结合,促进其酸化并激活NF-κB信号通路.
通过CHASERR激活NF-κB会导致神经炎症和神经元亡的增加.
抑制CHASERR抑制NF-κB的激活,并对大脑I/R损伤产生保护作用.

结论:

lncRNA-1810026B05Rik (CHASERR) 是通过NF-κB通路在脑I/R损伤中神经炎症和神经元亡的关键调节者.
沙塞尔在缺血性中风的发病过程中发挥着重要作用.
CHASERR代表了一种潜在的新型治疗点,用于中风治疗.

关键词:

的IκBα酸化.在 NF-κBB 中.大脑缺血症的大脑缺血症在ncRNA-1810026B05Rik中,我们可以使用

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