دورية أكاديمية
Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway
| العنوان: | Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway |
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| المؤلفون: | Ju Huang, Yu Zhu, Songtao Li, Huanyu Jiang, Nianzhi Chen, Hang Xiao, Jingwen Liu, Dan Liang, Qiao Zheng, Jianyuan Tang, Xiangrui Meng |
| المصدر: | Redox Report, Vol 28, Iss 1 (2023) |
| بيانات النشر: | Taylor & Francis Group, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Pathology LCC:Biology (General) |
| مصطلحات موضوعية: | Licochalcone B, Lipopolysaccharide, acute lung injury, oxidative injury, Inflammation, Oxidative stress, Pathology, RB1-214, Biology (General), QH301-705.5 |
| الوصف: | 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. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 13510002 1743-2928 1351-0002 |
| Relation: | https://doaj.org/toc/1351-0002; https://doaj.org/toc/1743-2928 |
| DOI: | 10.1080/13510002.2023.2243423 |
| URL الوصول: | https://doaj.org/article/c078970a416b448ab70d6841df683fbf |
| رقم الأكسشن: | edsdoj.078970a416b448ab70d6841df683fbf |
| قاعدة البيانات: | Directory of Open Access Journals |
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Full Text Finder | تدمد: | 13510002 17432928 |
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| DOI: | 10.1080/13510002.2023.2243423 |