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

作者全名："Huang, Ju; Zhu, Yu; Li, Songtao; Jiang, Huanyu; Chen, Nianzhi; Xiao, Hang; Liu, Jingwen; Liang, Dan; Zheng, Qiao; Tang, Jianyuan; Meng, Xiangrui"

作者地址："[Huang, Ju; Li, Songtao; Jiang, Huanyu; Liu, Jingwen; Liang, Dan; Zheng, Qiao; Tang, Jianyuan; Meng, Xiangrui] Hosp Chengdu Univ Tradit Chinese Med, Chengdu, Peoples R China; [Zhu, Yu] Chengdu Sport Univ, Chengdu, Peoples R China; [Chen, Nianzhi] Chongqing Med Univ, Coll Biomed Engn, State Key Lab Ultrasound Med & Engn, Chongqing, Peoples R China; [Xiao, Hang] Capital Med Univ, Beijing, Peoples R China; [Tang, Jianyuan; Meng, Xiangrui] Hosp Chengdu Univ Tradit Chinese Med, TCM Regulating Metab Dis Key Lab Sichuan Prov, Chengdu, Peoples R China"

通信作者："Tang, JY; Meng, XR (通讯作者)，Hosp Chengdu Univ Tradit Chinese Med, Chengdu, Peoples R China."

来源：REDOX REPORT

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:001048007000001

JCR分区：Q1

影响因子：5.2

年份：2023

卷号：28

期号：1

开始页：　

结束页：　

文献类型：Article

关键词：Licochalcone B; Lipopolysaccharide; acute lung injury; oxidative injury; Inflammation; Oxidative stress; Keap1; Nrf2 pathway; Therapeutic strategy

摘要："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."

基金机构："National Natural Science Foundation of China [82204778]; Science and Technology Department of Sichuan Province, China [2022YFG0145]; Sichuan Provincial Science and Technology Innovation Seedling Project [MZGC20230053]; central government guides local science and technology development projects of Sichuan Provincial Science and Technology Department [2021ZYD0107]"

基金资助正文："This work was supported by the National Natural Science Foundation of China [grant numbers: 82204778]; the Science and Technology Department of Sichuan Province, China [grant number: 2022YFG0145]; Sichuan Provincial Science and Technology Innovation Seedling Project [grant number: MZGC20230053]; the central government guides local science and technology development projects of Sichuan Provincial Science and Technology Department [grant number: No. 2021ZYD0107]."