Dehydrocorydaline attenuates bleomycin-induced pulmonary fibrosis by inhibiting fibroblast activation

作者：Jianhan He, Huihui Yue, Shufei Zhang, Ruihan Dong, Fengqin Zhang, Xuewen Wang, Ke Wang, Huilan Zhang, Dan‐Lei Yang, Zhaoxing Dong, Huiguo Liu · 发表于：Respiratory Research · 年份：2025 · DOI：10.1186/s12931-025-03218-5 · 被引用次数：5 · 研究领域：Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis、Lung Cancer Treatments and Mutations、Systemic Sclerosis and Related Diseases

BACKGROUND: Pulmonary fibrosis (PF) is an irreversible, progressive, chronic and fatal interstitial lung disease with limited therapeutic options. Dehydrocorydaline (DHC), derived from the traditional Chinese medicinal plant Corydalis yanhusuo, has exhibited a variety of pharmacological properties. Nevertheless, the potential function and mechanism of DHC in the management of PF have yet to be elucidated. PURPOSE: To evaluate the therapeutical efficacy of DHC in different PF models and elucidate its underlying mechanism. METHODS: A well-established Bleomycin-induced PF mouse model and human precision-cut lung slices (hPCLS) following fibrosis-inducing cocktail stimulation were employed. The antifibrotic effects of DHC on PF were measured by histopathological manifestation, immunofluorescent staining and expression levels of fibrosis related markers. Human primary pulmonary fibroblasts (HPFs) were used to explore the impact of DHC on fibroblast function and the underlying mechanism. RESULTS: Here, we demonstrated that DHC exhibited a therapeutic efficacy in Bleomycin-induced PF mouse model with a dose dependent, as well as in hPCLS after fibrosis-inducing cocktail stimulation, as evidenced by histopathological staining, decrease of Fibronectin, Collagen 1 and α-SMA expression. Additionally, in vitro experiments indicated that DHC effectively suppressed fibroblast to myofibroblast transition, but had no significant effect on the proliferation and migration of fibroblast. Mechan...