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

**Authors:** Xiaoyan Li, Bin Lv, Shumei Wang

PMC · DOI: 10.1186/s41065-025-00629-8 · 2025-12-27

## TL;DR

This study shows that Bufei Decoction, especially its component Schisandrin B, helps treat COPD by reducing lung damage and inflammation through a specific biological pathway.

## Contribution

The study identifies Schisandrin B as a key therapeutic component in Bufei Decoction that targets the TLR4/NF-κB/JAK-STAT pathway in COPD.

## Key findings

- Bufei Decoction dose-dependently improved lung function and reduced inflammation in COPD rats.
- Schisandrin B strongly binds to TLR4 and inhibits the NF-κB/JAK-STAT pathway, reducing lung injury and macrophage activation.
- TLR4 knockdown reversed the protective effects of Schisandrin B, confirming its role in the therapeutic mechanism.

## Abstract

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

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.

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.

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.

The online version contains supplementary material available at 10.1186/s41065-025-00629-8.

## Linked entities

- **Genes:** TLR4 (toll like receptor 4) [NCBI Gene 7099], JAK1 (Janus kinase 1) [NCBI Gene 3716], STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790]
- **Chemicals:** Schisandrin B (PubChem CID 108130), doxofylline (PubChem CID 50942)
- **Diseases:** COPD (MONDO:0005002)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}
- **Diseases:** COPD (MESH:D029424)
- **Chemicals:** Bufei (-), Schisandrin B (MESH:C015499)

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12853953/full.md

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Source: https://tomesphere.com/paper/PMC12853953