文章基本信息

标题：Semi-vioxanthin Isolated from Marine-Derived Fungus Regulates Tumor Necrosis Factor-α, Cluster of Differentiation (CD) 80, CD86, and Major Histocompatibility Complex Class II Expression in RAW264.7 Cells via Nuclear Factor-κB and Mitogen-Activated Protein Kinase Signaling Pathways
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作者：Xin-Ying Yang ; Sheng-Xin Cai ; Wen-Ji Zhang 等
期刊名称：Biological and Pharmaceutical Bulletin
印刷版ISSN：0918-6158
电子版ISSN：1347-5215
出版年度：2008
卷号：31
期号：12
页码：2228-2233
DOI：10.1248/bpb.31.2228
出版社：The Pharmaceutical Society of Japan
摘要：Semi-vioxanthin isolated from marine-derived fungus was assessed for immunoregulatory activity in mouse RAW264.7 macrophages. In the present study, the facilitative effects of semi-vioxanthin on tumor necrosis factor-α (TNF-α) and its mRNA expression and on expression of the co-stimulatory molecules, cluster of differentiation (CD) 80, CD86 and major histocompatibility complex class II (MHC II), as well as the molecular mechanism underlying the immunologic enhancement properties of semi-vioxanthin were studied. Our results clearly indicated that semi-vioxanthin treatment resulted in the degradation of IκBα, which led to the activation and nuclear translocation of the p65 subunit of nuclear factor-κB (NF-κB), as determined by immunoblotting, immunofluorescence and electrophoretic mobility shift assays (EMSA). Moreover, TNF-α production was prevented by NF-κB and mitogen-activated protein kinase (MAPK) inhibitors. Inhibition of NF-κB and extracellular signal regulated kinases (ERK1/2) activity by specific inhibitors blunted the effect of semi-vioxanthin on the up-regulation of CD80, CD86 and MHCII expression, but neither p38 MAPK nor c-Jun N-terminal kinase (JNK) inhibitor had this effect. Thus, we demonstrate that semi-vioxanthin regulates TNF-α production through NF-κB and MAPK signaling pathways. Activation of NF-κB and ERK1/2 were necessary for CD80, CD86 and MHCII expression induced by semi-vioxanthin. These data suggest that semi-vioxanthin has immunoregulatory effects.
关键词：semi-vioxanthin;tumor necrosis factor-α;co-stimulatory molecule;nuclear factor-κB;mitogen-activated protein kinase