ArticleChinese medicine2025
Isolinderalactone regulates macrophage polarization and efferocytosis by activating the LXRα pathway against ulcerative colitis.
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
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13 authors.
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Abstract
backgroundUlcerative colitis (UC), a chronic inflammatory bowel disease, remains an unmet medical need. Lindera aggregata, a traditional Chinese medicine used in treating gastrointestinal disorders, has demonstrated anti-UC efficacy, though its bioactive components are poorly characterized. Isolinderalactone (ILDL), a characteristic sesquiterpene lactone isolated from Lindera aggregata, has been demonstrated anti-cancer properties. However, its therapeutic potential in UC remains unexplored.
methodsLipopolysaccharide (LPS)-induced RAW264.7 inflammatory cell model was used to screen the anti-inflammatory properties of Lindera aggregata's characteristic compounds in vitro. DSS induced UC mouse model was used to study the anti-UC efficacy of ILDL in vivo. Transcriptomic was used to explore the anti-inflammatory mechanism of ILDL. Drug affinity responsible target stability was used to identify the combination of the ILDL and LXRα. LXR-mediated effects were further assessed via flow cytometry and Western blotting.
resultsILDL effectively inhibits macrophage polarization and the production of inflammatory mediators in vitro, and improves symptoms and tissue lesions in acute UC mice in vivo. Transcriptomic analysis revealed the involvement of the LXR-mediated pathway in ILDL's effects. Furthermore, ILDL was able to bind to LXRα and to upregulate LXRα target genes expression such as ABCA1, suggesting that ILDL itself can activate the LXRα pathway. Genetic/pharmacological LXRα inhibition abrogated ILDL's anti-inflammatory effects, confirming an LXRα-dependent mechanism. In addition to inhibiting macrophage M1 polarization, the activation of LXRα by ILDL can also promote macrophage efferocytosis of apoptotic intestinal epithelial cells in the co-culture system.
conclusionsILDL activates the LXRα pathway, inhibiting macrophage M1 polarization, reducing pro-inflammatory mediators production, and promoting macrophage efferocytosis. ILDL is a promising candidate compound from Lindera aggregata for anti-inflammation and UC treatment.
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