Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Shegan Mahuang Decoction ameliorates pulmonary fibrosis progression by inhibiting CCL3-mediated NETosis.
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Zhou Wencheng, Wang Zhisen, Du Haojie, Zhao Wanjun, Zhang Tao, Liu Zhengcheng, Qu Jiao, Sun Yang
Аннотация
BACKGROUND: Pulmonary fibrosis (PF) represents a spectrum of chronic lung disorders for which effective therapeutic options remain limited. Shegan Mahuang Decoction (SGMH) is a traditional Chinese medicine with potential therapeutic effects for respiratory system diseases. The precise mechanism of SGMH in treating PF has not yet been elucidated.
PURPOSE: This study aims to investigate the effectiveness and mechanism of SGMH in the treatment of PF.
METHODS: To investigate the effect of SGMH on PF, we established a mouse model and assessed inflammatory and neutrophil extracellular traps (NETs)-related markers. The target gene of SGMH was screened through integrated multi-omics analysis. The mechanisms of SGMH were explored through a series of experiments, encompassing NETs depletion with DNase I, the Pad4-/- mouse model, and pharmacological modulation via intraperitoneal administration of recombinant CCL3 (rCCL3) or a CCL3 neutralizing antibody (anti-CCL3).
RESULTS: SGMH ameliorated Bleomycin-induced lung tissue damage. It also inhibited pulmonary inflammation and NETs formation. Both DNase I-mediated NETs clearance and the Pad4-/- mice model showed that SGMH could not further ameliorate PF, indicating that SGMH blocks the PF development by inhibiting NETs formation. Multi-omics analysis and experimental validation found that SGMH inhibits NETs formation by targeting CCL3. Administration of rCCL3 restored NETs formation and attenuated the anti-fibrotic effect of SGMH. Moreover, treatment with anti-CCL3 alone inhibited PF, whereas its combination with SGMH did not further enhance the therapeutic effect.
CONCLUSION: This study demonstrated that SGMH ameliorates PF progression by inhibiting CCL3-mediated NETosis, suggesting its potential clinical application for PF treatment.
PURPOSE: This study aims to investigate the effectiveness and mechanism of SGMH in the treatment of PF.
METHODS: To investigate the effect of SGMH on PF, we established a mouse model and assessed inflammatory and neutrophil extracellular traps (NETs)-related markers. The target gene of SGMH was screened through integrated multi-omics analysis. The mechanisms of SGMH were explored through a series of experiments, encompassing NETs depletion with DNase I, the Pad4-/- mouse model, and pharmacological modulation via intraperitoneal administration of recombinant CCL3 (rCCL3) or a CCL3 neutralizing antibody (anti-CCL3).
RESULTS: SGMH ameliorated Bleomycin-induced lung tissue damage. It also inhibited pulmonary inflammation and NETs formation. Both DNase I-mediated NETs clearance and the Pad4-/- mice model showed that SGMH could not further ameliorate PF, indicating that SGMH blocks the PF development by inhibiting NETs formation. Multi-omics analysis and experimental validation found that SGMH inhibits NETs formation by targeting CCL3. Administration of rCCL3 restored NETs formation and attenuated the anti-fibrotic effect of SGMH. Moreover, treatment with anti-CCL3 alone inhibited PF, whereas its combination with SGMH did not further enhance the therapeutic effect.
CONCLUSION: This study demonstrated that SGMH ameliorates PF progression by inhibiting CCL3-mediated NETosis, suggesting its potential clinical application for PF treatment.