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沉默长非编码RNAX-无活性特异性转录减轻了Aβ1-42诱导的微质中介的神经毒性,通过转移微质M1/M2两极化

Kun-Peng Zhao¹, Xin-Yu Wang², Mei-Qi Shao²

¹Department of Geriatric Psychiatry, The Second Affiliated Hospital of Xinxiang Medical University, Henan Mental Hospital, Xinxiang, China.

International journal of immunopathology and pharmacology

|July 4, 2023

概括

长非编码RNAXIST下调缓解阿尔茨海默病的进展,通过调节微质极化. 这一过程涉及miR-107/PI3K/Akt通路,减少神经毒性.

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:

阿尔茨海默病 (AD) 是一种神经退行性疾病,其特点是逐渐认知能力下降.
微质激活和神经炎症在阿尔茨海默病的发病过程中起着至关重要的作用.
长非编码RNAs (lncRNAs) 正在成为各种疾病的关键调节者,包括AD.

研究的目的:

研究lncRNA XIST在阿尔茨海默氏病中微质极化和神经毒性的作用.
阐明涉及微RNA-107 (miR-107) 和PI3K/Akt信号通路的潜在分子机制.

主要方法:

定量实时PCR测量XIST和miR-107水平. 这是一个非常好的方法.
莫里斯水迷宫测试用于APP/PS1小鼠的认知功能评估.
免疫组织化学,西部斑,ELISA和细胞活力测试用于评估微质激活,极化和神经毒性.

主要成果:

在APP/PS1小鼠中,XIST水平升高,XIST沉默改善了AD的进展.
通过XIST knockdown,抑制了M1微质极化和促炎因素,同时促进了M2极化.
静音化XIST降低了Aβ1-42诱导的神经毒性和亡,可能通过miR-107/PI3K/Akt途径.

结论:

对XIST的下调减轻了AD中Aβ1-42诱导的微质中介的神经毒性.
通过XIST调节微质M1/M2极化是一个关键机制.
这种miR-107/PI3K/Akt通路与XIST在AD中的神经保护作用有关.

关键词:

阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.长非编码RNA X-无活性的特定转录.微质分极化微质分极化神经毒性的作用.

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