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Research Paper|Volume 14, Issue 16|pp 6626—6641

Oxypeucedanin relieves LPS-induced acute lung injury by inhibiting the inflammation and maintaining the integrity of the lung air-blood barrier

Li Du1, Jinrong Zhang2, Xiyue Zhang1, Chunyan Li1, Qi Wang1, Guangping Meng1, Xingchi Kan3, Jie Zhang1, Yuxi Jia4,5
  • 1Department of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, Jilin, China
  • 2Department of Pathogeny Biology, College of Basic Medical Sciences, Jilin University, Changchun, Jilin, China
  • 3Department of Theoretic Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, Jilin, China
  • 4Department of Orthopedics, The Second Hospital of Jilin University, Changchun, Jilin, China
  • 5Application Demonstration Center of Precision Medicine Molecular Diagnosis, The Second Hospital of Jilin University, Changchun, Jilin, China
Received: May 16, 2022Accepted: July 21, 2022Published: August 18, 2022
https://doi.org/10.18632/aging.204235

Copyright: © 2022 Du et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Introduction: Acute lung injury (ALI) is commonly accompanied by a severe inflammatory reaction process, and effectively managing inflammatory reactions is an important therapeutic approach for alleviating ALI. Macrophages play an important role in the inflammatory response, and this role is proinflammatory in the early stages of inflammation and anti-inflammatory in the late stages. Oxypeucedanin is a natural product with a wide range of pharmacological functions. This study aimed to determine the effect of oxypeucedanin on lipopolysaccharide (LPS)-induced ALI.

Methods and Results: In this study, the following experiments were performed based on LPS-induced models in vivo and in vitro. Using myeloperoxidase activity measurement, ELISA, qRT-PCR, and Western blotting, we found that oxypeucedanin modulated the activity of myeloperoxidase and decreased the expression levels of inflammatory mediators such as TNF-α, IL-6, IL-1β, MPO, COX-2 and iNOS in LPS-induced inflammation models. Meanwhile, oxypeucedanin inhibited the activation of PI3K/AKT and its downstream NF-κB and MAPK signaling pathways. In addition, oxypeucedanin significantly decreased the pulmonary vascular permeability, which was induced by LPSs, and the enhanced expression of tight junction proteins (Occludin and Claudin 3).

Conclusions: In conclusion, this study demonstrated that the anti-inflammatory mechanism of oxypeucedanin is associated with the inhibition of the activation of PI3K/AKT/NF-κB and MAPK signaling pathways and the maintenance of the integrity of the lung air-blood barrier.