白介素-17A介导的信号网络调控哮喘气道重塑的研究新进展

doi:10.12092/j.issn.1009-2501.2026.01.010

摘要/Abstract

摘要：

哮喘是气道免疫炎症性疾病，反复的炎症反应引起的“损伤-修复”致使气道结构发生重新塑造（即“重塑”），而气道重塑是哮喘患者肺功能不可逆性降低的主要原因。白介素-17A（IL-17A）作为IL-17的一个特殊亚型，在哮喘气道炎症、杯状细胞（GC）化生与黏蛋白（Muc）高表达以及平滑肌（ASM）增厚等气道重塑病理学变化过程中发挥了关键的调控作用，故IL-17A调控哮喘气道重塑相关信号网络已成为近年来研究的新热点。本文从视黄酸相关孤儿受体γt（RORγt）、信号转导与转录激活因子3（STAT3）、转化生长因子-β1（TGF-β1）、核因子-κB（NF-κB）以及p38丝裂原活化蛋白激酶（p38 MAPK）等信号网络的角度，综述IL-17A调控哮喘气道重塑的作用机制，为哮喘气道重塑机制研究以及新药研发提供理论依据。

关键词: 支气管哮喘, 气道重塑, 白介素-17A, 信号网络

Abstract:

Asthma is an immune inflammatory disease. Repeated inflammatory responses cause "damage-repair" to reshape the airway structure (known as "airway remodeling"), and airway remodeling is the main cause of irreversible reduction in lung function in asthma patients. Interleukin-17A (IL-17A), as a special subtype of IL-17, plays a key regulatory role in the pathological changes of airway remodeling, such as airway inflammation, goblet cell (GC) metaplasia, high expression of mucin (Muc), and smooth muscle (ASM) thickening in asthma. Therefore, IL-17A regulation of the signal network related to airway remodeling in asthma has become a new research hotspot in recent years. This article reviews the mechanism of IL-17A regulating airway remodeling in asthma from the perspective of signal networks such as retinoic acid-related orphan receptor γt (RORγt), signal transducer and activator of transcription 3 (STAT3), transforming growth factor-β1 (TGF-β1), nuclear factor-κB (NF-κB), and p38 mitogen-activated protein kinase (p38 MAPK), providing a theoretical basis for the study of the mechanism of airway remodeling in asthma and the development of new drugs.

Key words: bronchial asthma (asthma), airway remodeling, interleukin-17A, signaling network

中图分类号:

R562.25
R966

王志旺, 张悦, 全苹, 赵跃, 田蓓, 段海婧, 王瑞琼. 白介素-17A介导的信号网络调控哮喘气道重塑的研究新进展[J]. 中国临床药理学与治疗学, 2026, 31(1): 88-95.

Zhiwang WANG, Yue ZHANG, Ping QUAN, Yue ZHAO, Bei TIAN, Haijing DUAN, Ruiqiong WANG. Progress in the study of interleukin-17A-mediated signaling network regulating airway remodeling in asthma[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2026, 31(1): 88-95.

图/表 2

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信号网络	有效组分/ 小分子抑制剂	不同效应及组织病理变化	作用机制	参考文献
RORγt	CpG寡脱氧核苷酸	恢复Th17细胞免疫平衡；抑制气道上皮GC增生、Muc5ac高表达；减少沉积；气道壁变薄	下调RORγt、IL-17A表达	[14]
	人参皂苷Rg1	减轻炎症反应	IL-17A与RORγt表达下调	[15]
	BIX119（RORγt抑制剂）	缓解气道炎症反应；降低气道高反应性	抑制IL-17A/RORγt信号通路	[16]
STAT3	阳和平喘颗粒	减轻炎症细胞浸润；抑制上皮下胶原纤维沉积	IL-17A、 STAT3表达下调	[20]
STAT3	紫草素	抑制GC增生、Muc5ac高表达	下调IL-17A、p-STAT3的表达	[21]
TGF-β1	豆甾醇	减少炎症细胞数量；抑制ASMCs增殖	IL-17A、TGF-β1蛋白表达下调	[25]
TGF-β1	CpG寡脱氧核苷酸	气道壁变薄；减少胶原沉积	下调 IL-17A、TGF-β1表达	[27]
NF-κB	microRNA-133b	缓解气道黏液高分泌；ASM变薄	下调IL-17A、NF-κB表达	[31]
	BAY11-7082 （NF-κB小分子抑制剂）	减缓ASM紧张度；降低气道高反应性	抑制NF-κB核转位	[32]
	罗汉果苷V	减少炎症细胞浸润；抑制GC增生、ASMCs增殖；降低气道高反应性	阻断IL-17A/NF-κB信号通路	[33]
p38 MAPK	SB203580 （p38 MAPK抑制剂）	减轻气道炎症；抑制GC分化；Muc5ac高表达；提高气道顺应性	下调IL-17A、p38 MAPK 表达	[36]
	毛喉鞘蕊花提取物	抑制GC增生；减缓ASM紧张度	IL-17A、p38 MAPK表达下降	[37]
	合成生物碱	抑制ECM沉积	下调IL-17A/p38 MAPK信号通路	[38]
VEGF	茴香胶囊	降低气道胶原沉积占比；减缓支气管管壁紧张度；改善肺组织纤维化	IL-17A、VEGF mRNA表达下调	[40]
TNF-α	MRS5980 （腺苷受体激动剂）	抑制GC化生与胶原沉积；ASM变薄	IL-17A、TNF-α表达下调	[42]
NLRP3	MCC950 （NLRP3抑制剂）	减轻炎症反应	下调NLRP3炎症小体活性	[44]

信号网络	有效组分/ 小分子抑制剂	不同效应及组织病理变化	作用机制	参考文献
RORγt	CpG寡脱氧核苷酸	恢复Th17细胞免疫平衡；抑制气道上皮GC增生、Muc5ac高表达；减少沉积；气道壁变薄	下调RORγt、IL-17A表达	[14]
	人参皂苷Rg1	减轻炎症反应	IL-17A与RORγt表达下调	[15]
	BIX119（RORγt抑制剂）	缓解气道炎症反应；降低气道高反应性	抑制IL-17A/RORγt信号通路	[16]
STAT3	阳和平喘颗粒	减轻炎症细胞浸润；抑制上皮下胶原纤维沉积	IL-17A、 STAT3表达下调	[20]
STAT3	紫草素	抑制GC增生、Muc5ac高表达	下调IL-17A、p-STAT3的表达	[21]
TGF-β1	豆甾醇	减少炎症细胞数量；抑制ASMCs增殖	IL-17A、TGF-β1蛋白表达下调	[25]
TGF-β1	CpG寡脱氧核苷酸	气道壁变薄；减少胶原沉积	下调 IL-17A、TGF-β1表达	[27]
NF-κB	microRNA-133b	缓解气道黏液高分泌；ASM变薄	下调IL-17A、NF-κB表达	[31]
	BAY11-7082 （NF-κB小分子抑制剂）	减缓ASM紧张度；降低气道高反应性	抑制NF-κB核转位	[32]
	罗汉果苷V	减少炎症细胞浸润；抑制GC增生、ASMCs增殖；降低气道高反应性	阻断IL-17A/NF-κB信号通路	[33]
p38 MAPK	SB203580 （p38 MAPK抑制剂）	减轻气道炎症；抑制GC分化；Muc5ac高表达；提高气道顺应性	下调IL-17A、p38 MAPK 表达	[36]
	毛喉鞘蕊花提取物	抑制GC增生；减缓ASM紧张度	IL-17A、p38 MAPK表达下降	[37]
	合成生物碱	抑制ECM沉积	下调IL-17A/p38 MAPK信号通路	[38]
VEGF	茴香胶囊	降低气道胶原沉积占比；减缓支气管管壁紧张度；改善肺组织纤维化	IL-17A、VEGF mRNA表达下调	[40]
TNF-α	MRS5980 （腺苷受体激动剂）	抑制GC化生与胶原沉积；ASM变薄	IL-17A、TNF-α表达下调	[42]
NLRP3	MCC950 （NLRP3抑制剂）	减轻炎症反应	下调NLRP3炎症小体活性	[44]

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