Anti-Inflammatory Mechanisms of Koreanaside A, a Lignan Isolated from the Flower of Forsythia koreana, against LPS-Induced Macrophage Activation and DSS-Induced Colitis Mice: The Crucial Role of AP-1, NF-κB, and JAK/STAT Signaling
العنوان: | Anti-Inflammatory Mechanisms of Koreanaside A, a Lignan Isolated from the Flower of Forsythia koreana, against LPS-Induced Macrophage Activation and DSS-Induced Colitis Mice: The Crucial Role of AP-1, NF-κB, and JAK/STAT Signaling |
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المؤلفون: | Kyung-Tae Lee, Nam-In Baek, Kyung-Sook Chung, Tae Woo Kim, Yeong-Geun Lee, Ji-Sun Shin |
المصدر: | Cells Volume 8 Issue 10 Cells, Vol 8, Iss 10, p 1163 (2019) |
بيانات النشر: | MDPI, 2019. |
سنة النشر: | 2019 |
مصطلحات موضوعية: | 0301 basic medicine, Lipopolysaccharides, Male, Anti-Inflammatory Agents, Inflammatory bowel disease, NF-κB, chemistry.chemical_compound, Mice, 0302 clinical medicine, RAW 264.7 macrophages, STAT1, Glycosides, lcsh:QH301-705.5, DSS-induced colitis, Janus kinase 1, biology, Dextran Sulfate, NF-kappa B, JAK-STAT signaling pathway, General Medicine, Colitis, Nitric oxide synthase, STAT Transcription Factors, 030220 oncology & carcinogenesis, Tumor necrosis factor alpha, Signal Transduction, Flowers, Article, Lignans, Nitric oxide, 03 medical and health sciences, medicine, Animals, KA, Forsythia, Plant Extracts, Janus Kinase 1, Macrophage Activation, medicine.disease, AP-1, JAK/STAT, Mice, Inbred C57BL, Transcription Factor AP-1, 030104 developmental biology, RAW 264.7 Cells, lcsh:Biology (General), chemistry, Gene Expression Regulation, Cancer research, biology.protein |
الوصف: | The current treatment options for inflammatory bowel disease (IBD) are unsatisfactory. Therefore, novel and safer therapies are needed. We previously reported that koreanaside A (KA) showed high radical scavenging activity and suppressed vascular cell adhesion molecule 1 (VCAM-1) expression in vascular smooth muscle cells. However, the molecular mechanisms involved in its anti-inflammatory effect have not been reported. KA inhibited pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nitric oxide (NO), and prostaglandin E2 (PGE2). KA inhibited the production and mRNA expression of interleukin (IL)-6 and tumor necrosis factor-&alpha (TNF-&alpha ) induced by LPS. KA downregulated the myeloid differentiation primary response 88 (MyD88)-dependent inflammatory gene expressions in the MyD88-overexpressed cells. KA suppressed the LPS-induced transcriptional and DNA-binding activities of activator protein-1 (AP-1) and nuclear factor-kappa B (NF-&kappa B). KA was found to inhibit the phosphorylation of Janus kinase 1/2 (JAK1/2) and signal transducers and activators of transcription 1/3 (STAT1/3). In DSS-induced colitis mice, KA relieved the symptoms of colitis by suppressing inflammatory cell infiltration, restoring tight junction (TJ)- and epithelial&ndash mesenchymal transition (EMT)-related protein expression, and inactivating AP-1, NF-&kappa B, and STAT1/3. Therefore, KA reduced inflammatory responses by downregulating AP-1, NF-&kappa B, and JAK/STAT signaling in LPS-induced macrophages and DSS-induced colitis mice. |
وصف الملف: | application/pdf |
اللغة: | English |
تدمد: | 2073-4409 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::648324e0635947808aa0342b834d0e5fTest http://europepmc.org/articles/PMC6829247Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....648324e0635947808aa0342b834d0e5f |
قاعدة البيانات: | OpenAIRE |
تدمد: | 20734409 |
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