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超表达IL-1R1的M1型微细胞衍生的细胞外囊通过调节神经元炎症促进术后认知功能障碍

Zheng Qi^1,2, Yang Yu^1,2, Yu Su³

¹Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe Dong Road, Zhengzhou, 450000, People's Republic of China.

|July 28, 2023

概括

来自激活的M1型微质的细胞外囊泡通过促进神经元炎症和记忆力缺陷,恶化术后认知功能障碍 (POCD). 这些EVs有助于突触损失和神经元退化,突出POCD发展的新机制.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

手术后认知功能障碍 (POCD) 是手术和麻醉后的常见并发症,其特点是记忆障碍和认知能力下降.
激活的微质,特别是M1型,释放炎症因素,可以通过NF-κB信号传递等途径导致神经元损伤.
目前尚不完全了解POCD病原体的精确机制,需要对细胞和分子贡献者进行进一步的研究.

研究的目的:

研究来自M1型微质 (EVs^M1-Microglia) 的细胞外囊泡在POCD的病理过程中的作用.
在手术小鼠模型中阐明EVs^M1-Microglia对突触完整性,神经元退化和认知功能的影响.

主要方法:

在小鼠身上进行了手术以诱导POCD.
在海马神经元中测量了NF-κB酸化,IL-1β,PSD95和MAP2的水平.
评估了微细胞激活,突触结构以及EVs^M1-Microglia (带有和没有IL-1R1siRNA) 对神经元健康和记忆的影响.

主要成果:

手术显著增加NF-κB酸化和IL-1β,同时降低海马神经元中的PSD95和MAP2,表明神经元损伤和炎症.
手术诱导了微质激活,降低了突触密度,并导致神经元退化,这些影响被IL-1R1 siRNA部分减轻.
在手术小鼠中,EVs^M1-Microglia加剧了突触损失,神经元退化和记忆缺陷,独立于手术或微质激活本身.

结论:

来自M1型微质的细胞外囊泡 (EVs^M1-Microglia) 在促进POCD发育方面发挥着重要作用.
EVs,特别是具有高IL-1R1表达的EVs,通过诱导神经元炎症,突触损失和认知障碍,促进POCD.
针对EVs^M1-Microglia或它们的炎症信号通路,为缓解POCD提供了一个潜在的治疗策略.

关键词:

麻醉是一种麻醉.细胞外囊泡中的细胞外囊泡.术后认知功能障碍术后认知功能障碍手术手术手术手术手术手术手术

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