ArticleAnnals of translational medicine2020
Ruxolitinib protects lipopolysaccharide (LPS)-induced sepsis through inhibition of nitric oxide production in mice.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- In vivo inhibition of JAK-STAT signalling enhances high pathogenicity influenza virus replication in ducks.The Journal of general virology · 2026Article
- The Dual-Edged Sword: Risks and Benefits of JAK Inhibitors in Infections.Pathogens (Basel, Switzerland) · 2025Review
- From immune dysregulation to organ dysfunction: understanding the enigma of Sepsis.Frontiers in microbiology · 2024Review
- Review
- Coronavirus disease-2019: A review on the disease exacerbation via cytokine storm and concurrent management.International immunopharmacology · 2021Review
- Ruxolitinib Alleviates Uveitis Caused byMicroorganisms · 2021Article
- Drug repurposing and cytokine management in response to COVID-19: A review.International immunopharmacology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRuxolitinib is an inhibitor of Janus kinases (JAK) 1/2. It was authorised recently by the U.S. Food and Drug Administration (FDA) as a new Myelofibrosis treatment. In this study, we identified ruxolitinib as a new inhibitor of nitric oxide (NO) production in response to lipopolysaccharide (LPS)stimulation of RAW 264.7 cells.
methodsIn vitro direct effects of ruxolitinib were determined through NO production on RAW 264.7 cells. Also the expression level of iNOS, TNF-α and IL-6 were detected by Western Blotting and qRT-PCR. In vivo therapeutic effects of ruxolitinib on sepsis were evaluated by an endotoxemia model with C57 mice. The survival was calculated and histopathological damage of organs was observed by HE. Cytokines in serum were detected by Mouse Cytokine Array Panel.
resultsRuxolitinib was found to significantly reduce NO production, inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 expression, suggesting that ruxolitinib blocks LPS signaling that leads to pro-inflammatory factor expression. Furthermore, the inhibitory effects of ruxolitinib contributed to the survival of septic mice by 70% and pro-inflammatory cytokines in serum declined apparently. The results taken together indicate that ruxolitinib can significantly suppress LPS-stimulated NO production and improve the survival of septic mice, perhaps by interfering with the NF-κB pathway.
conclusionsThese findings suggest ruxolitinib might be a possible therapeutic candidate for sepsis therapy.
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