ArticleWorld journal of gastroenterology2026
Cedrol ameliorates ulcerative colitis
Article in World journal of gastroenterology, 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Chemical Profiling ofPharmaceuticals (Basel, Switzerland) · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUlcerative colitis (UC) is a chronic and treatment-resistant disorder requiring potent therapeutics that are effective and safe. Cedrol (CE) is a bioactive natural product present in many traditional Chinese medicines. It is known for its suppression of inflammation and mitigation of oxidative stress. Its therapeutic efficacy and mechanistic underpinnings in UC remain uncharacterized.
aimTo investigate the therapeutic potential and mechanisms of CE in UC.
methodsThe anti-inflammatory activity and intestinal barrier-repairing effects of CE were assessed in a dextran sulfate sodium-induced murine colitis model. Network pharmacology was employed to predict potential targets and pathways. Then molecular docking and dynamics simulations were utilized to confirm a stable interaction between CE and the toll-like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD2) complex. The anti-inflammatory mechanisms were further verified using
resultsCE significantly alleviated colitis symptoms, mitigated histopathological damage, and suppressed inflammation. Moreover, CE restored intestinal barrier integrity by enhancing mucus secretion and upregulating tight junction proteins (zonula occludens 1, occludin, claudin-1). Mechanistically, CE stably bound to MD2, inhibiting lipopolysaccharide-induced TLR4 signaling in RAW264.7 cells. This led to suppression of the downstream mitogen-activated protein kinase and nuclear factor kappa B signaling pathways, downregulating the expression of tumor necrosis factor-alpha, interleukin-1β, and interleukin-6. Gut microbiota analysis revealed that CE reversed dextran sulfate sodium-induced dysbiosis with significant enrichment of butyrogenic
conclusionCE acted on MD2 to suppress proinflammatory cascades, promoting mucosal barrier reconstitution and microbiota remodeling and supporting its therapeutic use in UC.
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