ArticleJournal of inflammation research2025
Upadacitinib Attenuates Lipopolysaccharide- and Cecal Ligation and Puncture-Induced Inflammatory Responses by Inhibiting NF-κB and Its Downstream Cytokines.
Article in Journal of inflammation research, 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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Who cites it
1 citing paper in PubMed.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Upadacitinib (UPA) is a selective tyrosine kinase 1 (JAK-1) inhibitor, which has been applied to treat atopic dermatitis, psoriatic arthritis, and ulcerative colitis in clinic. Whether it can treat sepsis remains unclear. Here, we investigate the effect of UPA on lipopolysaccharide (LPS)- and cecal ligation and puncture (CLP)-induced inflammatory responses in vitro and in vivo. Methods: In vitro, LPS-treated RAW264.7 cell line, LPS-treated TLR4 knock-out (TLR4 Results: In vitro, UPA significantly inhibited TLR4/NF-κB and JAK/STAT pathway in the LPS-treated RAW264.7 cells. In addition, UPA reduced protein expressions of NF-κB and its downstream inflammatory cytokines such as TNF-α, IL-1β in the LPS-treated TLR4 Conclusion: Taken together, UPA inhibits the LPS- and CLP-induced inflammatory responses in vitro and in vivo, which is associated with the inhibition of NF-κB and its downstream cytokines.
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