International immunopharmacology, 2017-12, Vol.53, p.149-157
2017
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- Autor(en) / Beteiligte
- Titel
- Oxymatrine protects against DSS-induced colitis via inhibiting the PI3K/AKT signaling pathway
- Ist Teil von
- International immunopharmacology, 2017-12, Vol.53, p.149-157
- Ort / Verlag
- Netherlands: Elsevier B.V
- Erscheinungsjahr
- 2017
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Oxymatrine (OMT), an alkaloid derived from the root of the Sophora flavescens, has been reported to possess a significant effect on relieving UC owing to its anti-inflammatory property. But the other therapeutic mechanism of OMT remains unclear. Recent studies have found, PI3K/AKT signaling pathway is involved in the pathogenesis of UC by pro-inflammatory effects and activating T cells. Moreover, PI3K/AKT pathway is one of the most important pathways for regulating cell apoptosis. Thus, we aim to explore whether OMT protects against UC by targeting PI3K/AKT pathway. We established the UC mice models, using LY294002 (a specific inhibitor of PI3K/AKT) as a positive control, to observe the effect of low, medium and high dose of OMT on UC and its influence on PI3K/AKT signaling pathway. Our data indicated that OMT can significantly ameliorate UC through anti-inflammatory, pro-apoptotic, down-regulating the differentiation of Th1 and Th17 cells via PI3K/AKT pathway. This study reveals that PI3K/AKT signaling pathway is a potential mechanism of OMT-induced UC remission and suggests that OMT is a promising therapeutic agent for the treatment of UC. [Display omitted] •Oxymatrine alleviates UC through regulating inflammation, apoptosis and immunity.•PI3K/AKT signaling pathway mediates the pathogenesis of UC.•Oxymatrine ameliorates UC by suppressing PI3K/AKT activation.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1567-5769eISSN: 1878-1705DOI: 10.1016/j.intimp.2017.10.025Titel-ID: cdi_proquest_miscellaneous_1961640759
- Format
- –
- Schlagworte
- 1-Phosphatidylinositol 3-kinase, AKT protein, Alkaloids - therapeutic use, Animal models, Animals, Anti-Inflammatory Agents - therapeutic use, Apoptosis, Cell Differentiation - drug effects, Cells, Cultured, Chemical compounds, Chromones - administration & dosage, Colitis, Colitis - chemically induced, Colitis - drug therapy, Colitis, Ulcerative - drug therapy, Dextran Sulfate, Disease Models, Animal, Helper cells, Humans, Immunity, Inflammation, Lymphocytes, Lymphocytes T, Male, Mice, Mice, Inbred BALB C, Morpholines - administration & dosage, Oncogene Protein v-akt - metabolism, Oxymatrine, Pathogenesis, Pharmacology, Phosphatidylinositol 3-Kinases - metabolism, PI3K/AKT pathway, Quinolizines - therapeutic use, Remission, Rodents, Signal transduction, Signal Transduction - drug effects, Signaling, Sophora - immunology, Studies, Th1 Cells - drug effects, Th1 Cells - immunology, Th17 Cells - drug effects, Th17 Cells - immunology, Ulcerative colitis