Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway

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...

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Main Authors: Ju Huang, Yu Zhu, Songtao Li, Huanyu Jiang, Nianzhi Chen, Hang Xiao, Jingwen Liu, Dan Liang, Qiao Zheng, Jianyuan Tang, Xiangrui Meng
Format: Article
Language:English
Published: Taylor & Francis Group 2023-12-01
Series:Redox Report
Subjects:
Online Access:https://www.tandfonline.com/doi/10.1080/13510002.2023.2243423
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author Ju Huang
Yu Zhu
Songtao Li
Huanyu Jiang
Nianzhi Chen
Hang Xiao
Jingwen Liu
Dan Liang
Qiao Zheng
Jianyuan Tang
Xiangrui Meng
author_facet Ju Huang
Yu Zhu
Songtao Li
Huanyu Jiang
Nianzhi Chen
Hang Xiao
Jingwen Liu
Dan Liang
Qiao Zheng
Jianyuan Tang
Xiangrui Meng
author_sort Ju Huang
collection DOAJ
description 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.
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spelling doaj.art-c078970a416b448ab70d6841df683fbf2023-12-09T20:05:02ZengTaylor & Francis GroupRedox Report1351-00021743-29282023-12-0128110.1080/13510002.2023.2243423Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathwayJu Huang0Yu Zhu1Songtao Li2Huanyu Jiang3Nianzhi Chen4Hang Xiao5Jingwen Liu6Dan Liang7Qiao Zheng8Jianyuan Tang9Xiangrui Meng10Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaChengdu sport university, Chengdu, People's Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, People’s Republic of ChinaCapital Medical University, Beijing, People’s Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People’s Republic of ChinaABSTRACTBackground 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.https://www.tandfonline.com/doi/10.1080/13510002.2023.2243423Licochalcone BLipopolysaccharide‌acute lung injuryoxidative injuryInflammationOxidative stress‌
spellingShingle Ju Huang
Yu Zhu
Songtao Li
Huanyu Jiang
Nianzhi Chen
Hang Xiao
Jingwen Liu
Dan Liang
Qiao Zheng
Jianyuan Tang
Xiangrui Meng
Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
Redox Report
Licochalcone B
Lipopolysaccharide‌
acute lung injury
oxidative injury
Inflammation
Oxidative stress‌
title Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
title_full Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
title_fullStr Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
title_full_unstemmed Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
title_short Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
title_sort licochalcone b confers protective effects against lps induced acute lung injury in cells and mice through the keap1 nrf2 pathway
topic Licochalcone B
Lipopolysaccharide‌
acute lung injury
oxidative injury
Inflammation
Oxidative stress‌
url https://www.tandfonline.com/doi/10.1080/13510002.2023.2243423
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