高流动性组盒子1 knockdown 抑制了EV71复制并通过TLR4/NF-κB/NLRP3轴减轻了细胞烧灭
Yufeng Zhang1, Jing Li1, Huiling Deng2
1Department of Infectious Diseases, Xi'an Children's Hospital, Xi'an, Shaanxi, China.
Journal of biochemical and molecular toxicology
|January 17, 2024
概括
高流动性组盒子1 (HMGB1) 减少抑制了Enterovirus 71 (EV71) 复制和烧灭. 通过向TLR4/NF-κB/NLRP3通路,降低HMGB1 Knockdown可以提高细胞活力并减少氧化应激.
科学领域:
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 肠道病毒71 (EV71) 导致手足口病 (HFMD),目前没有抗病毒治疗方法.
- 高流动性组盒1 (HMGB1) 在HFMD患者中被上调,但其在EV71感染中的作用尚不清楚.
研究的目的:
- 研究HMGB1在EV71感染中的作用和机制.
- 探索HMGB1对病毒复制,细胞活力,氧化应激和热的作用.
主要方法:
- 在患者和细胞模型中进行HMGB1表达分析 (RT-qPCR,西斑).
- 功能损失和功能增益实验,以评估HMGB1对EV71感染细胞的影响.
- 检测病毒标位,细胞活力,细胞循环,氧化应激和热.
主要成果:
- 在EV71感染的患者和细胞中,HMGB1水平升高,观察到核至细胞质转移.
- HMGB1的敲击抑制了EV71的复制,病毒蛋白的表达,并促进了抗病毒因素.
- 抑制HMGB1提高了细胞活力,防止了细胞循环停止,减少了氧化应激,并减弱了热亡.
- 过度表达HMGB1激活了TLR4/NF-κB/NLRP3通路,促进了烧灭.
结论:
- HMGB1在EV71的复制和发病过程中起着至关重要的作用.
- 抑制HMGB1通过TLR4/NF-κB/NLRP3通路减弱了EV71诱导的热和氧化应激.
- 向HMGB1可能提供针对EV71感染的治疗策略.
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