What question did this study set out to answer?

This study aims to explore the mechanisms by which Qingwen Baidu Decoction (QWBD) impacts acute lung injury (ALI) through the NLRP3 inflammasome pathway.

June 20, 2026

Mechanistic Study on the Treatment of Acute Lung Injury with Qingwen Baidu Decoction based on NLRP3 Inflammasome Signaling Pathway

Key Points

This study aims to explore the mechanisms by which Qingwen Baidu Decoction (QWBD) impacts acute lung injury (ALI) through the NLRP3 inflammasome pathway.
Identified bioactive constituents of QWBD using high-performance liquid chromatography (HPLC).
Established LPS-induced inflammatory models for therapeutic evaluation in vivo and in vitro.
Measured pulmonary edema severity, inflammatory cytokine levels, and conducted histopathological examinations.
Treatment with QWBD significantly reduced pulmonary edema compared to the LPS-treated group (W/D ratio not provided).
Showed improved alveolar structural integrity and decreased MPO activity and pro-inflammatory cytokines.
IHC/IF analyses indicated reduced expression of Caspase-1 and NLRP3 with corresponding downregulation of inflammasome-associated proteins confirmed by WB.

Abstract

INTRODUCTION: Qingwen Baidu Decoction (QWBD), a classical traditional Chinese medicine formula, has demonstrated clinical efficacy in managing acute lung injury (ALI). However, the precise mechanisms underlying its protective effects remain poorly characterized. METHODS: Major bioactive constituents of QWBD were identified through high-performance liquid chromatography (HPLC). Lipopolysaccharide (LPS)-induced in vivo and in vitro inflammatory models were established to evaluate therapeutic outcomes. Pulmonary edema severity was assessed via lung wet-to-dry weight ratio (W/D), while histopathological alterations were examined through hematoxylin-eosin (H&E) staining and transmission electron microscopy (TEM). Myeloperoxidase (MPO) activity and inflammatory cytokine levels were quantified to determine neutrophil activation and inflammatory responses. Mechanistic insights were obtained through immunohistochemistry (IHC), immunofluorescence (IF), and western blotting (WB) targeting the NLRP3 inflammasome pathway. RESULTS: HPLC analysis identified four principal bioactive components in QWBD. Treatment significantly attenuated pulmonary edema, ameliorated alveolar structural damage, and restored ultrastructural integrity of type II pneumocytes in ALI rats. QWBD significantly suppressed MPO activity and reduced pro-inflammatory cytokine levels compared to the LPS-treated group. IHC/IF revealed potent inhibition of cysteine-aspartic protease-1 (Caspase-1) and NOD-like receptor protein 3 (NLRP3) expression, while WB confirmed downregulation of NLRP3 inflammasome- associated proteins. DISCUSSION: QWBD alleviates ALI by inhibiting NLRP3 inflammasome activation and upstream regulators, thereby attenuating pro-inflammatory cytokine maturation. Its multi-component composition confers advantages over single-target agents while potentially avoiding the broad immunosuppression associated with dexamethasone. Clinical validation of its therapeutic potential remains warranted. CONCLUSION: QWBD protects against ALI by implying NLRP3 inflammasome suppression, demonstrating promise as a multi-targeted therapy for inflammatory lung disorders.

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