Rhizoma coptidis can inhibit the excessive proliferation, inflammation, and transformation of lung fibroblasts into myofibroblasts

Main Article Content

Jie Yang
Yuting Huang
Zhimin Cui
Chang Liu
Guofang Xie


Rhizoma coptidis (COP), FMT, inflammation, Nrf2/HO-1 pathway, pulmonary fibrosis (PF)


Background: Pulmonary fibrosis (PF) is a chronic, progressive, and irreversible heterogeneous disease of lung interstitial tissue. To combat progression of PF, new drugs are required to be developed. Rhizoma coptidis (COP), one of the main alkaloids of Coptis chinensis, is a traditional herbal medicine used to treat various inflammatory diseases.

Objective: To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.

Material and Methods: Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.

Results: Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.

Conclusion: Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.

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