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Objective <p>Evaluate Bufei Decoction effects on chronic obstructive pulmonary disease (COPD) and elucidate Schisandrin B (Sch B) mechanism via TLR4 pathway.</p> Methods <p>COPD was induced in rats using LPS/cigarette smoke. Effects of low, medium, high-dose Bufei Decoction and doxofylline were assessed on lung pathology, function, blood gases, and inflammation. Sch B role was investigated via network pharmacology (identifying active components/targets), molecular docking (schisandrin B-TLR4 binding), and in vivo validation.</p> Results <p>Bufei Decoction dose-dependently ameliorated COPD-induced lung injury, improved pulmonary function/blood gases, and reduced inflammation (high-dose most effective). Network pharmacology identified 241 Bufei Decoction components (including Sch B) targeting core molecules (TLR4, JAK1, STAT3). Molecular docking confirmed strong Sch B-TLR4 binding. Functional analysis implicated immune/inflammatory pathways. In vivo experiments showed that Sch B dose-dependently alleviated lung injury, improved pulmonary function, reduced the levels of inflammatory markers, and inhibited the M1/M2 macrophage ratio as well as the expression of proteins related to the NF-κB/JAK-STAT signaling pathway. Crucially, TLR4 knockdown reversed Sch B’s protective effects, worsening injury and inflammation.</p> Conclusions <p>Bufei Decoction treats COPD through multi-component synergy. Sch B is a key active component, exerting therapeutic effects by targeting TLR4 to regulate macrophage polarization and inhibit the NF-κB/JAK-STAT signaling pathway, thereby improving lung function and reducing inflammation.</p>

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Investigating the therapeutic mechanism of Bufei Decoction in COPD: Schisandrin B targets the TLR4/NF-κB/JAK-STAT signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月27日

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  • Xiaoyan Li,
  • Bin Lv,
  • Shumei Wang

摘要

Objective

Evaluate Bufei Decoction effects on chronic obstructive pulmonary disease (COPD) and elucidate Schisandrin B (Sch B) mechanism via TLR4 pathway.

Methods

COPD was induced in rats using LPS/cigarette smoke. Effects of low, medium, high-dose Bufei Decoction and doxofylline were assessed on lung pathology, function, blood gases, and inflammation. Sch B role was investigated via network pharmacology (identifying active components/targets), molecular docking (schisandrin B-TLR4 binding), and in vivo validation.

Results

Bufei Decoction dose-dependently ameliorated COPD-induced lung injury, improved pulmonary function/blood gases, and reduced inflammation (high-dose most effective). Network pharmacology identified 241 Bufei Decoction components (including Sch B) targeting core molecules (TLR4, JAK1, STAT3). Molecular docking confirmed strong Sch B-TLR4 binding. Functional analysis implicated immune/inflammatory pathways. In vivo experiments showed that Sch B dose-dependently alleviated lung injury, improved pulmonary function, reduced the levels of inflammatory markers, and inhibited the M1/M2 macrophage ratio as well as the expression of proteins related to the NF-κB/JAK-STAT signaling pathway. Crucially, TLR4 knockdown reversed Sch B’s protective effects, worsening injury and inflammation.

Conclusions

Bufei Decoction treats COPD through multi-component synergy. Sch B is a key active component, exerting therapeutic effects by targeting TLR4 to regulate macrophage polarization and inhibit the NF-κB/JAK-STAT signaling pathway, thereby improving lung function and reducing inflammation.