ArticleInflammopharmacology2024
Baricitinib relieves DSS-induced ulcerative colitis in mice by suppressing the NF-κB and JAK2/STAT3 signalling pathways.
Article in Inflammopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 10 citations in OpenAlex.
- Supernatants of Water Extraction-Ethanol Precipitation from Roots ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Honokiol and Magnolol Exert an Anti-Inflammatory Effect by Inhibiting JAK2/STAT3/IL17 Signalling in a Rat Model of Ulcerative Colitis: A Combination of Bioinformatics and Experimental Study.Journal of cellular and molecular medicine · 2026Article
- Naringin ameliorates intestinal injury in ulcerative colitis model mice by modulating the JAK2/STAT3 signaling pathway.Molecular medicine reports · 2026Article
- Baricitinib Augments Lonafarnib Therapy to Preserve Colonic Homeostasis and Microbial Balance in a Mouse Model of Progeria.Aging cell · 2025Article
- Identification of shared and unique mechanisms of atopic dermatitis and ulcerative colitis by construction and computational analysis of disease maps.Computational and structural biotechnology journal · 2025Article
- Targeting Interferon-Gamma (IFN-γ)-Related Signalling Pathways in Inflammatory Bowel Disease: Emerging Inhibitors and Therapeutic Advances.Mediators of inflammation · 2025Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Ulcerative colitis (UC) is a relapsing inflammatory disease with a unique aetiology. The treatment of UC is challenging, and the current clinical therapeutics for colitis have limited efficacy. Thus, finding new and effective treatment options remains urgent. Baricitinib, an inhibitor of Janus kinase (JAK), has been clinically used to treat rheumatoid arthritis (RA). However, its potential effects on UC have not been fully elucidated. In this study, we aimed to explore the effects of baricitinib on UC and its underlying mechanism. Dextran sulphate sodium (DSS)-induced murine model of chronic colitis was used to investigate the intervention efficacy following oral administration of baricitinib. The levels of key cytokines, such as IL-6, IFN-γ and IL-17A, were determined. Moreover, western blotting for IκBα, p-IκBα, JAK2, p-JAK2, STAT3 and p-STAT3 protein expression was performed to investigate the associated signalling pathways. Our findings demonstrated that baricitinib can significantly relieve DSS-induced UC in mice. After baricitinib intervention, IL-6, IFN-γ and IL-17A levels were decreased both in vitro and in vivo. Moreover, the elevated expression levels of p-IκBα, p-JAK2, and p-STAT3 were significantly reduced after treatment. Collectively, these results suggest that baricitinib is a potential therapeutic agent for alleviation of DSS-induced colitis. This study provides a method for subsequent investigations on potential curative drugs development of the for colitis.
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