Emodin alleviates LPS-induced inflammatory response in lung injury mice by affecting the function of neutrophils

Abstract

Background: This study aims to investigate the role of Emodin(Emo) on the pulmonary inflammatory response and the neutrophil function in a murine model of lipopolysaccharide (LPS)-induced ALI. The mouse model of lipopolysaccharide (LPS)-induced ALI was produced by acute lung injury of injecting 20 mg/kg LPS via the caudal vein.The right lower lung lobes were harvested, fixed,embedded and stained with hematoxylin and eosin (H&E) for light microscopy analysis to evaluate lung injury. TNF-αand IL-1 ELISA kits were used to detect the levels of TNF-α and IL-1 in the right lung homogenate of rats. The primary rat neutrophils were separated and treated with LPS to mimic a ALI cellular model. The expression of Respiratory burst and Neutrophil NETs Production was examined using spectrophotometer.The Elastase release was detected using Elastase Activity Assay kit.The ROS Production was measured by Luminometer.the phagocytosis of Neutrophils and the rate of apoptotic Neutrophils were measured by flow cytometry. Results: This study demonstrates that Emo alleviates lung injury and reduces the release of inflammatory cytokines. Moreover, Emo also downregulated neutrophil respiratory burst and the production of ROS in the LPS-stimulated neutrophils, thus reducing the damage of neutrophils to the surrounding tissues. Emo can also up-regulate the ability of neutrophils to phagocytize bacteria and generate NETs, thereby enhancing the bactericidal ability of neutrophils. In addition, Emo can promote the apoptosis of neutrophils and accelerate the resolution of inflammation. Conclusion: Emo has a protection effect on LPS-induced acute lung injury mice. It can alleviate lung injury and reduces the release of inflammatory cytokines, perhaps by affecting the various function of neutrophils in a dose-dependent manner.