LncRNA HOTAIR通过激活NF-κB通路来促进LPS诱导的炎症反应
Fengqing Zhu1, Zexun Mo1, Wuzhou Lin1
1Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong, China.
Experimental biology and medicine (Maywood, N.J.)
|January 22, 2026
概括
长非编码RNAHOTAIR通过NF-κB通路促进炎症,从而加剧急性肺损伤 (ALI). 沉默HOTAIR为ALI治疗提供了一个潜在的治疗策略.
科学领域:
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 急性肺损伤 (ALI) 涉及由NF-κB信号通路驱动的过度炎症.
- 长非编码RNAs (lncRNAs) 越来越多地被认为在炎症性疾病中的作用.
研究的目的:
- 为了研究 lncRNA HOTAIR 在脂聚糖 (LPS) 诱导的 ALI 中的作用.
- 评估HOTAIR作为ALI的潜在治疗点.
主要方法:
- 利用LPS诱导的肺损伤的A549细胞和小鼠模型.
- 评估HOTAIR表达,细胞活力,促炎性细胞因子水平 (IL-1β,IL-6,TNF-α).
- 分析了NF-κB信号通路的激活 (IκBα和p65酸化,p65核转位) 和HOTAIR敲击效应.
主要成果:
- 在A549细胞中,LPS增加了HOTAIR表达,降低了细胞活力,并增加了A549细胞中的促炎细胞因子.
- 霍泰尔过度表达放大了NF-κB信号;霍泰尔沉默扭转了这些效应.
- 在体内,HOTAIR knockdown减轻了小鼠的肺损伤,减少了炎症,并抑制了NF-κB的激活.
结论:
- 在ALI中,HOTAIR有助于NF-κB驱动的炎症性损伤.
- 霍泰尔在ALI的发病过程中起着调节作用.
- 准HOTAIR为ALI提供了一个潜在的治疗途径.
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