ArticleFrontiers in pharmacology2025
Ruxolitinib alleviates DSS-induced acute ulcerative colitis by inhibiting STAT1 phosphorylation and reducing MDSC infiltration.
Article in Frontiers in pharmacology, 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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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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1 citing paper in PubMed.
- Identification of Pyrrolo [2,3-Molecules (Basel, Switzerland) · 2026Article
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4 authors.
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Abstract
Objective: This study aimed to evaluate the therapeutic effects of Ruxolitinib, a JAK1/2 inhibitor, on DSS-induced acute colitis in mice, with a focus on its impact on disease activity, inflammatory responses, modulation of myeloid-derived suppressor cells (MDSCs), and regulation of the JAK/STAT1 signaling pathway. Methods: Acute UC was induced in C57BL/6 mice by administering a 2.5% DSS solution. Mice were randomly assigned to three groups: the blank group (no DSS), the model group (DSS only), and the Ruxolitinib-treated group (DSS +30 mg/kg Ruxolitinib by gavage for 14 consecutive days). Body weight, disease activity index (DAI) scores, spleen weight, and colon length were measured. Spleen index and the spleen weight-to-colon length ratio were calculated. Flow cytometry was used to assess the proportion of MDSCs in the blood. Results: Conclusion: Ruxolitinib effectively ameliorated DSS-induced acute colitis by reducing inflammation, modulating MDSC levels, and inhibiting STAT1 activation. These findings suggest that Ruxolitinib could be a promising therapeutic agent for UC, targeting both the immune response and the JAK/STAT1 signaling pathway.
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