Non-targeted Metabonomics Study of Epicatechin on Acute Lung Injury Induced by Lipopolysaccharide in BALB/c Mice

PurposeTo study the regulatory effect of epicatechin (EC) on the inflammation of acute lung injury (ALI) in mice.

MethodA suction-type tracheal instillation method was used to establish ALI model in BALB/c mice. The histopathological changes were observed, based on the non-target metabonomics methods by ultra-high performance liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (HILIC UHPLC-Q-TOF MS) were studied on lung tissue.

ResultCompared with the control group, significant inflammatory changes were observed in lung tissue of mice treated with lipopolysaccharide (LPS), however, it was slight in pretreatment EC group. Metabolic profile analysis of lung tissue demonstrated that 20-hydroxy arachidonic acid, tryptophan, phenylalanine, tyrosine, ATP, choline, 20-tetradecenoic acid, phosphoric acid, enol, and glucose diphosphate were closely related to endogenous metabolism in ALI of mice. They might involve six metabolic pathways such as glyceride metabolism, glycolysis, phospholipid metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, ascorbic acid and metabolism, and choline metabolism.

ConclusionThe study investigated the mechanism of effect of epicatechin intervention on ALI by non-targeted metabonomics method, which provided a theoretical basis for anti-inflammatory property of epicatechin.