Jingfang granules inhibiting LPS-induced acute lung injury via regulating linoleic acid and arachidonic acid metabolism pathway

TL;DR

This study explores how Jingfang Granules reduce acute lung injury by regulating fatty acid metabolism pathways in a rat model.

Contribution

The study identifies specific metabolites and pathways regulated by Jingfang Granules in treating acute lung injury.

Findings

JFG regulated 12 blood metabolites, including arachidonic and linoleic acids, in LPS-induced ALI rats.

Eleven urine metabolites were affected, mainly linked to fatty acid and amino acid metabolism pathways.

JFG intervention restored pathways related to inflammation and fatty acid metabolism in ALI.

Abstract

Acute lung injury (ALI) is a severe clinical syndrome with high mortality. Jingfang Granules (JFG), a modern formulation of the traditional Chinese medicine (TCM) compound Jingfang Baidu Powder, has been widely used to treat ALI. However, its protective effects and underlying mechanisms in ALI remain poorly understood. This study is based on a lipopolysaccharide (LPS)-induced ALI rat model, which was intervened with low, medium, and high dose of JFG. We carried out metabolomic analysis and identified 12 blood metabolites, the levels of core metabolites were regulated under JFG intervention, including L-Carnitine, Citric acid, Taurocholic acid, Arachidonic acid (AA), and Linoleic Acid (LA). Besides blood metabolites, 11 urine metabolites were also callback under JFG intervention, including Valine, Citric acid, L-Phenyalalanine, and Leukotriene B4, mainly involving the LA metabolism, AA metabolism, and phenylalanine, tyrosine and tryptophan biosynthesis. Comprehensive analysis shows that the restored enrichment pathways are mainly concentrated in inflammatory response, amino acid metabolism, and fatty acid metabolism. These findings reveal the potential mechanism of JFG in LPS-induced ALI, and its pathway nodes facilitate rapid translation from laboratory to clinical applications.

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