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NEAT1/miR-181a-5p/HMGB1轴在败血症模型中调节巨细胞极化和炎症

Kuo Wang¹, Yancun Liu², Yanfen Chai³

¹Tianjin Medical University General Hospital; Department of Critical Care Medicine, Affiliated Hospital of Hebei University.

Journal of visualized experiments : JoVE

|February 2, 2026

概括

长非编码RNANEAT1调节了败血症中的巨细胞两极分化. 沉默NEAT1通过调节miR-181a-5p/HMGB1通路,减少炎症和组织损伤,有利于败血症小鼠.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
遗传学遗传学是一个

背景情况:

败血症涉及免疫调节失调和高死亡率.
长非编码RNANEAT1在败血症引起的巨细胞两极分化中的作用尚不清楚.
了解NEAT1的功能对于败血症治疗至关重要.

研究的目的:

在败血症中研究NEAT1/miR-181a-5p/HMGB1轴.
确定NEAT1对巨细胞极化和败血症进展的影响.
建立一个方法框架,用于研究在败血症中ceRNA网络.

主要方法:

使用定量PCR,西部抹杀和双露西法酶记者分析.
在NEAT1,miR-181a-5p和HMGB1.1之间确认了竞争性内源性RNA (ceRNA) 相互作用.
采用了体外 (培养的巨细胞) 和体内 (CLP小鼠模型) 的研究,包括功能测定和组织病理学.

主要成果:

NEAT1和HMGB1被上调,而miR-181a-5p在败血症患者和刺激的巨细胞中被下调.
NEAT1沉默促进了M2巨细胞的两极分化,并减少了促炎性细胞因子.
在小鼠中,NEAT1 knockdown缓解了败血症引起的组织损伤和受损的巨细胞迁移.

结论:

NEAT1/miR-181a-5p/HMGB1轴在败血症的发病过程中发挥着重要作用.
针对NEAT1提供了潜在的败血症治疗策略.
这项研究提供了一种新型的综合协议,用于表征感染中lncRNA-microRNA-HMGB1调节电路.

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