ArticleJournal of inflammation research2024
Mechanism of Qingdai in Alleviating Acute Lung Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- PLB1 enhances adhesion and invasion of Trichosporon asahii to lung epithelial cells: insights into the mechanisms of Cav1/JAK/STAT3-induced arginine metabolism.Respiratory research · 2026Article
- Selective JAK2 inhibition by TG101209 reprograms macrophage polarization and alleviates acute lung injury.Frontiers in immunology · 2026Article
- Epigallocatechin-3-gallate ameliorates lipopolysaccharide-induced inflammation via the 67LR/JAK2/STAT3 signaling pathway.Scientific reports · 2025Article
- Integrating multi-dimensional data to reveal the mechanisms and molecular targets of baikening granules for treatment of pediatric influenza.Frontiers in molecular biosciences · 2025Article
- Regulated programmed cell death in acute lung injury: from pathogenesis to therapy.Frontiers in immunology · 2025Review
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Authors and funding
9 authors.
Funding
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Abstract
Objective: Qingdai (QD) is a traditional Chinese medicine (TCM) commonly used in clinical practice to treat acute lung injury/acute respiratory distress syndrome (ALI/ARDS). However, the mechanisms underlying the effects of QD remain not fully understood. This investigation demonstrated QD alleviated LPS-induced ALI in mice and exerted anti-inflammatory effects by inhibiting the JAK2/STAT3 signaling pathway. Methods: The active compounds of QD were identified through UPLC-LTQ-Orbitrap-MS/MS. Network pharmacology predicted potential pharmacological targets and the signaling pathways contributed to the effectiveness of QD in treating ALI. Molecular docking assessed the binding of active components to critical targets. ALI mice triggered by Lipopolysaccharides (LPS) were used for transcriptomic analysis to assess alterations in pulmonary gene expression. The pathological changes of lung tissue were analyzed via HE staining. Proinflammatory cytokine levels in serum were measured using ELISA, and the mRNA expression was measured by RT-qPCR. Western blot analysis evaluated protein expression related to the JAK2/STAT3 signaling pathway. Additionally, RAW264.7 cells induced by LPS were treated with QD to measure proinflammatory cytokines and JAK2/STAT3 signaling pathway protein expression. Results: Six major components of QD were identified. Network pharmacology predicted JAK2 and STAT3 as targets for QD in ALI treatment, with KEGG analysis highlighting the JAK/STAT signaling pathway. Transcriptomics confirmed the JAK/STAT signaling pathway in the therapeutic effects of QD. Molecular docking demonstrated high binding affinities of bisindigotin, isoindigo, and 6-(3-oxoindolin-2-ylidene)indolo[2,1-b]quinazolin-12-one (IQO) to JAK2 and STAT3. In vivo, QD reduced lung inflammation, downregulated proinflammatory cytokines, and inhibited JAK2/STAT3 signaling pathway. In vitro, QD mitigated LPS-triggered inflammatory responses in RAW264.7 macrophages by inhibiting the same pathway. Conclusion: The therapeutic effects of QD in ALI might be mediated by the modulation of the JAK2/STAT3 signaling pathway, which may make it a valuable therapeutic strategy for ALI/ARDS.
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