在过敏性鼻炎中,HMGB1通过促进BECN1-介导的自,损害鼻膜上皮质屏障功能
Zhaoen Ma1, Langrui Tu1, Xiaobin Yang1
1Department of Otolaryngology, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Biochemistry and biophysics reports
|November 28, 2025
概括
高流动性组盒子1 (HMGB1) 通过自破坏鼻上皮屏障,使过敏性鼻炎 (AR) 恶化. 针对HMGB1-BECN1通路可能提供新的AR治疗方法.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 呼吸系统医学 呼吸系统医学
背景情况:
- 高流动性组盒1 (HMGB1) 是一种促进炎症的细胞因子,会损害鼻膜上皮质屏障的功能.
- 过敏性鼻炎 (AR) 涉及显著的上皮屏障功能障碍.
研究的目的:
- 阐明HMGB1在AR上皮质屏障损伤中的机制性作用.
- 调查自的参与HMGB1介导的屏障功能障碍.
主要方法:
- 在人类鼻上皮细胞 (hNEpiC) 中的HMGB1敲击.
- 评估自标志物 (例如LC3B).
- 对上皮屏障功能的测量 (TEER,FITC-dextran透性,紧结蛋白).
- 路西法雷斯记者测定以评估BECN1促销者活动.
- BECN1沉默的实验. 沉默的实验.
主要成果:
- 降低HMGB1抑制了自标志物,并赋予了对IL-4诱导的屏障功能障碍的抵抗力.
- HMGB1激活了BECN1促进体,表明了转录调节.
- BECN1沉默取消了HMGB1诱导的自和屏障破坏.
结论:
- HMGB1通过激活BECN1-依赖的自而关键调解AR进展.
- HMGB1-BECN1-自轴代表了AR管理的潜在治疗目标.
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