HPLC analysis of QWBD and the mechanism by which it improves acute lung injury

Abstract Relevance Qingwen Baidu Decoction (QWBD) is a traditional Chinese medicine that has been used to cure infectious diseases. Previous studies have confirmed that QWBD possesses significant anti-inflammatory and heat-clearing effects, but the specific underlying mechanism remains unclear. Aim of the study: This study used QWBD to investigate the molecular pathways underlying lipopolysaccharide (LPS)-induced acute lung injury (ALI). Materials and methods Network pharmacology was used to predict the targets and pathways of QWBD in ALI, as well as the binding activity and molecular docking. HPLC was used to validate the methodology, identify the chemical components, and identify the active constituents of QWBD. The rat model of ALI was induced by LPS. The water content of the lungs, TNF-α and IL-1β levels, and myeloperoxidase (MPO) and HMGB1 expression were measured to reflect the anti-inflammatory propertiesof QWBD in ALI rats. Pathological sections were prepared to measure the effect of QWBD on ALI. Western blotting was performed to measure the expression of TLR4, Myd88, HMGB1, p-JNK, p-AKT, p-PI3K, JNK, PI3K, and AKT and to identify the underlying mechanism. In cell experiments, serum pharmacochemical methods were used to reproduce LPS-induced cell damage. Drug-containing serum QWBD was used to measure NO, TNF-α, and IL-1β levels and fluorescence localization of HMGB1. Results: HPLC indicated that the main components of QWBD were quercetin, kaempferol, luteolin, baicalin, gardenoside, mangiferin, and ferulic acid, which conformed to the predicted results of network pharmacology. QWBD downregulated cytokine production in ALI rats, reduced inflammation, and protected against lung tissue damage. QWBD hindered the nuclear translocation of inflammatory transcription factors and decreased cytokine production in Raw264.7 inflammatory cells. The expression of TLR4, MYD88, HMGB1, P-JNK, P-AKT, and P-PI3K was decreased at the molecular level. Conclusions: QWBD suppressed the inflammatory response in the rat model of ALI through the TLR4/JNK and PI3K/AKT signaling pathways.