ArticleRedox report : communications in free radical research2023
Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway.
Article in Redox report : communications in free radical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Ethanolic Extract ofAntioxidants (Basel, Switzerland) · 2026Article
- Exploring the protective mechanisms and therapeutic potential of carnosic acid against acute respiratory distress syndrome through molecular docking, molecular dynamics and experimental verification.Experimental and therapeutic medicine · 2026Article
- Control of inflammatory lung injury and repair by metabolic signaling in endothelial cells.Current opinion in hematology · 2025Review
- Licochalcone B suppresses oxidative stress and apoptosis accompanied by upregulating Nrf2/HO-1 pathway to ameliorate diabetic nephropathy in mice.Frontiers in pharmacology · 2025Article
- Investigating the protective effects of fluvoxamine against sepsis-related acute lung injury through antiapoptotic, anti-inflammatory, and anti-oxidant features in rats.Iranian journal of basic medical sciences · 2025Article
- The role of Keap1-Nrf2 signaling pathway in the treatment of respiratory diseases and the research progress on targeted drugs.Heliyon · 2024Review
- Article
- Glycyrrhizin alleviates BoAHV-1-induced lung injury in guinea pigs by inhibiting the NF-κB/NLRP3 Signaling pathway and activating the Nrf2/HO-1 Signaling pathway.Veterinary research communications · 2024Article
- 3-methyladenine ameliorates acute lung injury by inhibiting oxidative damage and apoptosis.Heliyon · 2024Article
- Article
- Article
- Therapeutic potential and action mechanisms of licochalcone B: a mini review.Frontiers in molecular biosciences · 2024Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute 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.
methodsWe 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.
resultsLCB 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.
conclusionLCB 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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