期刊
NUTRITION RESEARCH
卷 35, 期 3, 页码 241-250出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.nutres.2015.01.001
关键词
Inflammation; glucosylceramide; cyclooxygenase-2; NF-kappa B; MAPKs; macrophage
资金
- Technology Development Program for Food, Ministry for Food, Agriculture, Forestry and Fisheries, Sejong-si, Republic of Korea [109108-3]
- Basic Science Research Program through National Research Foundation of Korea - Ministry of Education, Science and Technology, Sejong-si [2012R1A1A3014565, 2013R1A1A2008487]
- National Research Foundation of Korea [2013R1A1A2008487, 2012R1A1A3014565] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
The positive effect of glucosylceramide (GlcCer) on skin conditions is well known. Recently, there has been increasing interest in the potential antiinflammatory effects of GlcCer due to its efficacy in relieving atopic skin symptoms. However, the role of GlcCer in inflammation has not been investigated completely. Thus, we hypothesized that GlcCer might exhibit the antiinflammatory effects through the inhibition of nuclear factor kappa B (NF-kappa B) and mitogen-activated protein kinase (MAPK) signaling. To test this hypothesis, the antiinflammatory effects and signaling mechanisms of GlcCer were investigated in lipopolysaccharide (LPS)-induced RAW 264.7 cells. We report that GlcCer inhibited messenger RNA and protein expression of tissue necrosis factor alpha and interleukin 1 beta without cytotoxicity. However, it did not affect interleukin 6 production in LPS-stimulated RAW 264.7 macrophages. Glucosylceramide also suppressed prostaglandin E-2 but not nitric oxide production, consistent with its inhibition of cyclooxygenase 2 but not of inducible nitric oxide synthase expression. The molecular mechanism of GlcCer-mediated inhibition of LPS-induced inflammation in RAW 264.7 cells is closely related to suppression of NF-kappa B p65 subunit nuclear translocation as well as to phosphorylation of extracellular signal-regulated kinase and, in particular, p38 MAPK. In addition, GlcCer did not affect c-Jun N-terminal kinase phosphorylation. In conclusion, GlcCer inhibits LPS-induced inflammation by blocking the nuclear translocation of NF-kappa B and inhibiting the phosphorylation of extracellular signal-regulated kinase/p38 MAPK pathways in macrophages, suggesting that it might be a promising potential drug candidate for various inflammatory diseases. (C) 2015 Elsevier Inc. All rights reserved.
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