ArticleAllergy, asthma & immunology research2025
Inotodiol Attenuates Mucosal Inflammation in a Mouse Model of Eosinophilic Chronic Rhinosinusitis.
Article in Allergy, asthma & immunology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Article
- Lidocaine-Based Derivatives for the Treatment of Staphylococcal Enterotoxin B-Induced Chronic Rhinosinusitis.International journal of molecular sciences · 2025Article
- From functional foods to immunotherapeutic agents: mechanistic insights into medicinal mushroom bioactives in chronic inflammation management.Frontiers in nutrition · 2025Review
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9 authors.
Funding
Abstract
purposeInotodiol (22-hydroxy lanosterol), a unique component of chaga mushrooms, is believed to be a medicinal component with reported antitumor, antiviral, and anti-inflammatory properties. This study evaluated the therapeutic potential and underlying mechanisms of inotodiol in eosinophilic chronic rhinosinusitis (ECRS).
methodsAn ECRS mouse model was established using female BALB/c mice. Forty mice were categorized into 4 groups: the control group (n = 10), ECRS group treated with solvent (n = 10), ECRS group treated with inotodiol 20 mg/kg (n = 10), and ECRS group treated with dexamethasone 10 mg/kg (n = 10). The nasal lavage fluid and tissue samples from mice were analyzed for cytokine and chemokine expression as well as for the severity of mucosal inflammation. Enzyme-linked immunosorbent assay, quantitative reverse transcription-polymerase chain reaction, histopathological staining, and immunofluorescence techniques were employed. The human eosinophil cell line (EoL-1) and dispersed nasal polyp cells (DNPCs) were used to assess inotodiol-induced eosinophil apoptosis
resultsInotodiol significantly reduced the secretion of T2 cytokine and mast cell tryptase as well as the expression of Th cytokines, chemokines, and proinflammatory/inflammatory cytokines in ECRS mice. Furthermore, it suppressed mucosal inflammatory features such as polyp formation, epithelial thickening, and eosinophil infiltration. Inotodiol treatment reduced mast cell activation and increased eosinophil apoptosis in the nasal mucosa of ECRS mice. Notably, inotodiol also induced apoptosis in EoL-1 cells and DNPCs, which may contribute to its anti-inflammatory effects.
conclusionsInotodiol could be a potential therapeutic agent for ECRS by modulating immune responses and reducing mucosal inflammation.
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