中国麻风皮肤病杂志 ›› 2026, Vol. 42 ›› Issue (4): 247-253.doi: 10.12144/zgmfskin202604247

• 论著 • 上一篇    下一篇

苯并芘通过AhR/Notch通路调控脂质合成在化脓性汗腺炎发病中的作用与机制研究

阮丹丹,胡婷婷,杨雪帆,李嘉祺,莫小辉,鞠强   

  1. 上海交通大学医学院附属仁济医院皮肤科，上海，200127
  • 出版日期:2026-04-15 发布日期:2026-04-07

Role and mechanism of benzo(a)pyrene in regulating lipid synthesis via the AhR/Notch pathway in the pathogenesis of hidradenitis suppurativa

RUAN Dandan, HU Tingting, YANG Xuefan, LI Jiaqi, MO Xiaohui, JU Qiang   

  1. Department of Dermatology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China
  • Online:2026-04-15 Published:2026-04-07

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摘要： 目的：探讨吸烟影响化脓性汗腺炎（HS）发生的可能分子机制。方法：以苯并芘［benzo(a)pyrene,BaP］处理HaCaT 细胞模拟香烟暴露，通过芳香烃受体（aryl hydrocarbon receptor, AhR)小干扰RNA（siRNA）及 Notch 通路抑制剂（DAPT）探究调控机制。采用qRT-PCR 和 Western Blot 检测 Notch 通路及脂质代谢相关基因（FASN、SREBP1）的表达；利用尼罗红染色及CCK-8法分别评估HaCaT细胞脂质合成能力和细胞活力；并结合单细胞转录组测序分析吸烟与非吸烟HS患者皮损中表皮角质形成细胞Notch 通路的表达差异。结果：BaP 处理显著抑制 HaCaT 细胞中 NOTCH1 表达并减少脂质合成，Notch通路抑制剂（DAPT）可产生类似效应。机制研究证实，BaP 通过 AhR 调控 NOTCH1 表达，敲低 AhR 部分恢复BaP 对 NOTCH1 的抑制作用。单细胞转录组测序证实，与不吸烟患者相比，吸烟 HS 患者皮损表皮角质形成细胞Notch 通路呈下调趋势。结论：香烟中的BaP通过AhR抑制Notch通路并影响细胞脂质合成，这可能是吸烟加重 HS 的潜在分子机制之一。

关键词: 苯并芘, 化脓性汗腺炎, 芳香烃受体, Notch, 角质形成细胞

Abstract: Objective: To explore the possible molecular mechanisms by which cigarette smoking influences the pathogenesis of hidradenitis suppurativa (HS). Methods: To simulate cigarette smoke exposure, HaCaT cells were treated with benzo(a)pyrene (BaP). The underlying regulatory mechanisms were investigated using aryl hydrocarbon receptor (AhR)-siRNA and the Notch pathway inhibitor DAPT. The expression of genes related to the Notch pathway and lipid metabolism (specifically FASN and SREBP1) was quantified via qRT-PCR and Western Blot. Nile Red staining and CCK-8 assays were employed to evaluate lipid synthesis capacity and cell viability, respectively. Furthermore, single-cell RNA sequencing was utilized to analyze expression differences in the Notch pathway within epidermal keratinocytes between smoking and non-smoking patients with HS. Results: BaP treatment significantly inhibited NOTCH1 expression and reduced lipid synthesis in HaCaT cells, an effect mirrored by the Notch inhibitor DAPT. Mechanistic studies confirmed that BaP regulates NOTCH1 expression through the AhR. Notably, siRNA-mediated knockdown of AhR partially rescued the BaP-induced suppression of NOTCH1. Consistent with these in vitro findings, single-cell RNA sequencing analysis demonstrated a down-regulation of Notch pathway in the lesional keratinocytes of smoking HS patients compared to non-smoking counterparts. Conclusion: BaP in cigarette smoke inhibits the Notch pathway and cellular lipogenesis via an AhR-dependent manner, which could be one of the underlying molecular mechanisms by which smoking exacerbates HS.

Key words: benzo(a)pyrene, hidradenitis suppurativa, aryl hydrocarbon receptor, Notch, keratinocytes