ABSTRACT
Background
Acute lung injury (ALI) is a severe and often fatal pulmonary disease. Current treatments for ALI and acute respiratory distress syndrome (ARDS) are limited. Natural product metabolites have shown promise as therapeutic alternatives. However, the effects of Licochalcone B (LCB) on ALI are largely unknown.
Methods
We investigated the effects of LCB on lipopolysaccharide-challenged mice and human pulmonary microvascular endothelial cells. Cell viability, apoptosis, and ROS production were assessed. Lung tissue histopathology and oxidative stress and inflammation markers were evaluated. Protein expression levels were measured.
Results
LCB had no cytotoxic effects on cells and increased cell viability. It reduced apoptosis and ROS levels in cells. In mice with ALI, LCB decreased lung tissue weight and improved oxidative stress and inflammation markers. It also enhanced expression levels of Nrf2, HO-1, and NQO1 while reducing Keap1.
Conclusion
LCB protects against LPS-induced acute lung injury in cells and mice. The Keap1/Nrf2 pathway may be involved in its protective effects. LCB shows potential as a strategy to alleviate ALI caused by LPS.
Acknowledgements
Ju Huang contributed to the preparation of the figures and tables, and writing of the manuscript. Yu Zhu, Songtao Li and Nianzhi Chen contributed to data collection and preparation of Figures and Tables. Huangyu Jiang, Jingwen Liu, Niang Dan, Hang Xiao and Qiao Zheng reviewed the manuscript. Jianyuan Tang and Xiangrui Meng contributed to the establishment of the structure of this manuscript and acted as the main supervisor. All authors read and approved the final manuscript.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Ethics statement
All animal procedures were approved by the Animal Care and Use Committee of Chengdu University of Traditional Chinese Medicine (2023-04).
Data availability statement
The authors confirm that the data supporting the findings of this study are available within the article [and/or] its supplementary materials.