Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
Ju Huang,
Yu Zhu,
Songtao Li,
Huanyu Jiang,
Nianzhi Chen,
Hang Xiao,
Jingwen Liu,
Dan Liang,
Qiao Zheng,
Jianyuan Tang,
Xiangrui Meng
Affiliations
Ju Huang
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Yu Zhu
Chengdu sport university, Chengdu, People's Republic of China
Songtao Li
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Huanyu Jiang
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Nianzhi Chen
State Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, People’s Republic of China
Hang Xiao
Capital Medical University, Beijing, People’s Republic of China
Jingwen Liu
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Dan Liang
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Qiao Zheng
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Jianyuan Tang
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
Xiangrui Meng
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of China
ABSTRACTBackground 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.
