ArticleScientific reports2015
Chronic inflammation up-regulates P-gp in peripheral mononuclear blood cells via the STAT3/Nf-κb pathway in 2,4,6-trinitrobenzene sulfonic acid-induced colitis mice.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 49 citations in OpenAlex.
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- Mesalazine alleviated the symptoms of spontaneous colitis in interleukin-10 knockout mice by regulating the STAT3/NF-κB signaling pathway.World journal of gastroenterology · 2025Article
- Health Benefits of Electrolyzed Hydrogen Water: Antioxidant and Anti-Inflammatory Effects in Living Organisms.Antioxidants (Basel, Switzerland) · 2024Review
- High and Low Levels ofInternational journal of molecular sciences · 2023Article
- Unlocking Drug Resistance in Multiple Myeloma: Adipocytes as Modulators of Treatment Response.Cancers · 2023Article
- Regulation of P-Glycoprotein in the Brain.International journal of molecular sciences · 2022Review
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- Steroid Resistance Associated with High MIF and P-gp Serum Levels in SLE Patients.Molecules (Basel, Switzerland) · 2022Article
- Efflux capacity and aldehyde dehydrogenase both contribute to CD8+ T-cell resistance to posttransplant cyclophosphamide.Blood advances · 2022Article
- P-glycoprotein: new insights into structure, physiological function, regulation and alterations in disease.Heliyon · 2022Review
- Paeonol Protects Against Methotrexate-Induced NephrotoxicityFrontiers in pharmacology · 2022Article
- Anti-inflammatory activities ofFrontiers in pharmacology · 2022Article
- How Macrophages Become Transcriptionally Dysregulated: A Hidden Impact of Antitumor Therapy.International journal of molecular sciences · 2021Review
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
Patients with inflammatory bowel diseases, including Crohn's disease and ulcerative colitis, often suffer drug intolerance. This resistance can be divided into intrinsic resistance and acquired resistance. Although there is agreement on acquired resistance, studies regarding intrinsic resistance have demonstrated inconsistencies, especially for Crohn's disease. For this reason, an animal model of Crohn's disease was induced with 2,4,6-trinitrobenzene sulfonic acid solution (TNBS), and intrinsic resistance was analyzed by measuring the function and expression of P-glycoprotein (P-gp) in peripheral mononuclear blood cells (PMBC), followed by mechanistic studies. The results revealed reduced retention of cyclosporine A in PMBC over-expressing P-gp in a TNBS-treated group and enhanced secretion of the cytokines IL-1β, IL-6, IL-17, and TNF-α as well as LPS in plasma. These cytokines and LPS can induce P-gp expression through the STAT3/Nf-κb pathway, contributing to a decrease of cyclosporine A retention, which can be reversed by the application of a P-gp inhibitor. Our results demonstrated that the sustained chronic inflammation could induce the intrinsic resistance presented as P-gp over-expression in PBMC in Crohn's disease through STAT3/Nf-κb pathway and this resistance might be reversed by combinational usage of P-gp inhibitors.
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