香烟烟雾提取物诱导RELMβ通过NF-κB/p65信号传递在慢性阻塞性肺病中的炎症
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Jiaxin Lin1, Hua Liao1, Xingdong Cai1
1Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Annals of clinical and laboratory science
|November 18, 2025
概括
香烟烟雾提取物 (CSE) 在慢性阻塞性肺病 (COPD) 中增加了类似抵抗素的β分子 (RELMβ). RELMβ通过NF-κB/p65通路促进炎症,有助于COPD的进展.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 慢性阻塞性肺病 (COPD) 是一种渐进的肺病.
- 香烟烟雾提取物 (CSE) 是COPD发病的主要原因之一.
- 抗类分子β (RELMβ) 在COPD中CSE诱导的炎症中的作用需要进一步阐明.
研究的目的:
- 研究CSE对COPD中RELMβ表达的调控作用.
- 阐明RELMβ调节COPD炎症因子的机制.
- 通过RELMβ.65确定NF-κB/p65信号通路在CSE诱导的炎症中的参与.
主要方法:
- 在CSE暴露后,在16HBE细胞中评估了RELMβ表达.
- 在RELMβ操纵的16HBE细胞中评估了NF-κB/p65激活,IκBα降解和炎症因子表达.
- 使用NF-κB信号通路抑制剂 (pyrrolidine dithiocarbamate,Bay 11-7082) 来阻止CSE和RELMβ的影响.
主要成果:
- 在16HBE细胞中,CSE暴露提高了RELMβ的mRNA和蛋白质表达.
- 过度表达或刺激RELMβ增强了关键炎症性细胞因子 (IL-1β,IL-8,IL-6,TNF-α) 的分泌和mRNA表达.
- CSE和RELMβ激活了NF-κB/p65通路,通过增加酸化,核转位和IκBα降解来证明,这种降解被NF-κB抑制剂阻断.
结论:
- 通过调节RELMβ,从而激活NF-κB/p65信号通路,CSE诱导COPD的炎症.
- 在COPD中,RELMβ在调解CSE诱导的炎症反应方面发挥着重要作用.
- 这项研究提供了对CSE对通过RELMβ.的COPD进展的贡献背后的分子机制的新见解.
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