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

Year: 2025
Type: article
Abstract: 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.
Source: Hereditas
DOI: 10.1186/s41065-025-00629-8
Language: English
Field: Medicine
Open Access status: gold
Estimated APC paid: $2,590
OpenAlex ID: W7117355663
FWCI: 0.608
Cites: 45
Cited by: 1
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