Wen Yang Ding Chuan Tang Attenuates Asthmatic Airway Remodeling by Inhibiting M2 Macrophage-Driven Fibroblast Activation

Li-Li Sun; Zhu-Ying Li; Rui Jiang; Chun-Yan Li; Ping Wu; Tao Chi; Lian-Yan Cui; Dong-Xue Wang

doi:10.3791/69737

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Research Article

Wen Yang Ding Chuan Tang Attenuates Asthmatic Airway Remodeling by Inhibiting M2 Macrophage-Driven Fibroblast Activation

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DOI:

10.3791/69737

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March 24th, 2026

Li-Li Sun¹ , Zhu-Ying Li² , Rui Jiang¹ , Chun-Yan Li³ , Ping Wu¹ , Tao Chi⁴ , Lian-Yan Cui⁵ , Dong-Xue Wang⁶

¹Department of Traditional Chinese Medicine, The Third Affiliated Hospital of Qiqihar Medical University, ²Department of Respiratory, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, ³Department of Clinical Pharmacy, The Third Affiliated Hospital of Qiqihar Medical University, ⁴Department of Central Laboratory, The Third Affiliated Hospital of Qiqihar Medical University, ⁵Department of Stomatology, The Third Affiliated Hospital of Qiqihar Medical University, ⁶Department of Magnetic Resonance, The Third Affiliated Hospital of Qiqihar Medical University

Summary

This article describes a study on the regulation of pulmonary fibroblast fibrosis by Wenyang Dingchuan Decoction through inhibition of M2 macrophage polarization.

Abstract

To study the effects of Wen Yang Ding Chuan Tang (WYDCT) on fibroblast function, airway remodeling in asthma, and the underlying mechanism. IL-4 was used to induce M2 polarization of RAW264.7 macrophages, and the polarized macrophages were then treated with WYDCT to investigate its effect on mouse lung fibroblasts. Polarized RAW264.7 cells were subjected to different treatments and then co-cultured with fibroblasts. M1 and M2 marker levels, cell morphology, and IL-6 concentration were assessed. STAT3 protein level was analyzed. Fibroblast viability, proliferation, colony formation, PCNA expression, and the expression of fibronectin, COL1A1, and α-SMA were analyzed using various assays, including real-time PCR, Western blot, CCK-8, Edu, immunofluorescence, and colony formation assays. WYDCT reversed the IL-4-induced morphological changes in RAW264.7 cells, reduced the levels of M2 markers (Arg-1, CD206) and IL-6, and decreased STAT3 expression in RAW264.7 cells, while supplementation with IL-6 restored the effect of WYDCT on M2 markers. Furthermore, WYDCT inhibited fibroblast viability and proliferation, reduced PCNA expression, and decreased fibrosis markers (fibronectin, COL1A1, α-SMA), suggesting that WYDCT inhibits the viability, proliferation, and fibrosis of lung fibroblasts by suppressing macrophage M2 polarization, in which the IL-6/STAT3 signaling pathway may play a key role.

Introduction

Asthma, also known as bronchial asthma, is a persistent inflammatory condition of the respiratory passages¹. Frequently linked to allergen exposure, cold temperatures, and irritants of both physical and chemical nature, this condition is characterized by infiltration of inflammatory cells, reversible constriction of airways, mucus secretion, and bronchospasm². Currently, there are at least 300 million asthma patients worldwide, and the prevalence is increasing year by year³. In 2015, 400,000 people died from asthma, making it a serious global health issue⁴^,