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Protection against Lipopolysaccharide-Induced Endotoxemia by Terrein Is Mediated by Blocking Interleukin-1β and Interleukin-6 Production

التفاصيل البيبلوغرافية
العنوان: Protection against Lipopolysaccharide-Induced Endotoxemia by Terrein Is Mediated by Blocking Interleukin-1β and Interleukin-6 Production
المؤلفون: Yeo Dae Yoon, Myeong Youl Lee, Byeong Jo Choi, Chang Woo Lee, Hyunju Lee, Joo-Hee Kwon, Jeong-Wook Yang, Jong Soon Kang
المصدر: Pharmaceuticals, Vol 15, Iss 11, p 1429 (2022)
بيانات النشر: MDPI AG, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine
LCC:Pharmacy and materia medica
مصطلحات موضوعية: terrein, endotoxemia, interleukin-1β, interleukin-6, NF-κB, Medicine, Pharmacy and materia medica, RS1-441
الوصف: Terrein is a fungal metabolite and has been known to exert anti-melanogenesis, anti-cancer, and anti-bacterial activities. However, its role in endotoxemia has never been investigated until now. In the present study, we examined the effect of terrein on lipopolysaccharide (LPS)-induced endotoxemia in mice and characterized the potential mechanisms of action. Treatment with terrein increased the survival of mice and decreased the production of inflammatory cytokines, including interleukin-1β (IL-1β) and interleukin-6 (IL-6) in an LPS-induced endotoxemia model. In addition, terrein suppressed the LPS-induced production of IL-1β and IL-6 in RAW 264.7 cells, a murine macrophage-like cell line, and the mRNA expression of IL-1β and IL-6 was also inhibited by terrein in LPS-stimulated RAW 264.7 cells. Further study demonstrated that terrein blocked LPS-induced phosphorylation of p65 subunit of nuclear factor (NF)/κB and the phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) was also suppressed by terrein treatment. Collectively, these results suggest that terrein exerts a protective effect again LPS-induced endotoxemia in mice by blocking the production of inflammatory cytokines. Our results also suggest that the anti-inflammatory effect of terrein might be mediated, at least in part, by blocking the activation of NF-κB, JNK, and p38 MAPK signaling pathways.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1424-8247
Relation: https://www.mdpi.com/1424-8247/15/11/1429; https://doaj.org/toc/1424-8247
DOI: 10.3390/ph15111429
URL الوصول: https://doaj.org/article/20818632003d450b97efea768d2737df
رقم الأكسشن: edsdoj.20818632003d450b97efea768d2737df
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14248247
DOI:10.3390/ph15111429