Diammonium glycyrrhizinate lipid ligand ameliorates lipopolysaccharide?induced acute lung injury by modulating vascular endothelial barrier function

The aim of the present study was to investigate effects diammonium glycyrrhizinate lipid ligand (DGLL) treatment on acute lung injury (ALI) and pulmonary edema induced by lipopolysaccharide (LPS) in Sprague?Dawley rats. Rats orally received 30, 60 120 mg/kg DGLL. After 1 h, rat ALI model established LPS (10 mg/kg) intraperitoneal injection. 6 evaluated using hematoxylin eosin staining techniques. Pulmonary wet?dry weight ratio, protein concentrations bronchoalveolar lavage fluid (BALF) Evans blue (EB) extravasation tissue. expression levels tumor necrosis factor (TNF)?? interleukin (IL)?1? tissues were measured ELISA. Myeloperoxidase (MPO) detected immunohistochemical staining. Western blotting used measure level changes intercellular adhesion molecule (ICAM)?1, as well adherent tight junction proteins, including vascular endothelial (VE)?cadherin, zonula occludens (ZO)?1, occludin junctional (JAM)?1 that associated with inflammation microvascular permeability. DGLL significantly alleviated LPS, which demonstrated reduction MPO?positive cells TNF??, IL?1? ICAM?1 tissues. In addition, abrogated LPS?induced edema, decreased concentration BALF reduced EB extravasation. also reversed VE?cadherin ZO?1, JAM?1 caused LPS. conclusion, exhibits a protective effect ALI, is inhibition inflammatory cell infiltration barrier disruption. results provide theoretical basis for application potential clinical ALI.