Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages
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초록
We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability tosuppress inflammatory responses as well as the molecularmechanisms underlying these abilities, using lipopolysaccharide(LPS)-stimulated RAW264.7 cells. Salicortin inhibitediNOS expression and the subsequent production of NO in adose-dependent manner in the LPS-stimulated RAW 264.7cells. Salicortin significantly suppressed LPS-induced signalcascades of NF-κB activation, such as IKK activation, IκBαphosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation ofJNK, but not ERK or p38 MAPK. Furthermore, salicortinsignificantly inhibited production of pro-inflammatory cytokines,such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW264.7 cells. These findings suggest that salicortin may show itsanti-inflammatory activity by suppressing the LPS-inducedexpression of pro-inflammatory mediators through inhibitionof NF-κB and JNK MAPK signaling cascades in macrophages.
Abstract
We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability tosuppress inflammatory responses as well as the molecularmechanisms underlying these abilities, using lipopolysaccharide(LPS)-stimulated RAW264.7 cells. Salicortin inhibitediNOS expression and the subsequent production of NO in adose-dependent manner in the LPS-stimulated RAW 264.7cells. Salicortin significantly suppressed LPS-induced signalcascades of NF-κB activation, such as IKK activation, IκBαphosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation ofJNK, but not ERK or p38 MAPK. Furthermore, salicortinsignificantly inhibited production of pro-inflammatory cytokines,such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW264.7 cells. These findings suggest that salicortin may show itsanti-inflammatory activity by suppressing the LPS-inducedexpression of pro-inflammatory mediators through inhibitionof NF-κB and JNK MAPK signaling cascades in macrophages.
참고문헌 (22)
- Pierce, G. F., "Macrophages: important physiologic and pathologic sources of polypeptide growth factors", Am. J. Respir. Cell Mol. Biol, 2, pp.233~234 (1990)
- Marks-Konczalik, J., "Cytokine-mediated transcriptional induction of the human inducible nitric oxide synthase gene requires both activator protein 1 and nuclear factor kappaB-binding sites", J. Biol. Chem, 273, pp.22201~22208 (1998)
- Yang, F., "IKKβplays an essential role in the phosphorylation of RelA", p65 on serine 536 induced by lipopolysaccharide, 2003, pp.170, 5630~5635
- 이지애, "Differential regulation of inducible nitric oxide synthase and cyclooxygenase-2 expression by superoxide dismutase in lipopolysaccharide stimulated RAW 264.7 cells", Experimental and Molecular Medicine, 41(9), pp.629~637 (2009), 생화학분자생물학회
- Ben-Neriah, Y., "Inflammation meets cancer, with NF-κB as the matchmaker", Nat. Immunol, 12, pp.715~723 (2011)
- Donath, M. Y., "Type 2 diabetes as an inflammatory disease", Nat. Rev. Immunol, 11, pp.98~107 (2011)
- Guha, M., "LPS induction of gene expression in human monocytes", Cell Signal, 13, pp.85~94 (2001)
- Karin, M., "The IκB kinase (IKK) and NF-κB: key elements of proinflammatory signaling", Semin. Immunol, 12, pp.85~98 (2000)
- Gloire, G., "NF- kappaB activation by reactive oxygen species: fifteen years later", Biochem. Pharmacol, 72, pp.1493~1505 (2006)
- Kaminska, B., "MAPK signalling pathways as molecular targets for anti-inflammatory therapy--from molecular mechanisms to therapeutic benefits", Biochim. Biophys. Acta, 1754, pp.253~262 (2005)
- Martineau, L. C., "Anti-adipogenic activities of Alnus incana and Populus balsamifera bark extracts, part II: bioassay-guided identification of actives salicortin and oregonin", Planta Med, 76, pp.1519~1524 (2010)
- Yang, H., "Neuroprotective compounds from Salix pseudo-lasiogyne twigs and their anti-amnesic effects on scopolamine-induced memory deficit in mice", Planta Med, 79, pp.78~82 (2013)
- Lee, H. J., "Phenolicglycosides as inhibitors of inducible nitric oxide synthase from Populus davidiana in LPS-activated RAW 264 .7 murine macrophages", Pharmazie, 67, pp.870~873 (2012)
- Knuth, S., "Catechol, a bioactive degradation product of salicortin, reduces TNF-α induced ICAM-1 expression in human endothelial cells", Planta Med, 77, pp.1024~1026 (2011)
- Kim, S. Y., "Transduced PEP-1-FK506BP inhibits the inflammatory response in the Raw 264.7 cell and mouse models", Immunobiology, 216, pp.771~781 (2011)
- Barnes, P. J., "Nuclearfactor-kappaB: a pivotal transcription factor in chronic inflammatory diseases", N. Engl. J. Med, 336, pp.1066~1071 (1997)
- Uto, T., "6-(Methylsulfinyl) hexyl isothiocyanate suppresses inducible nitric oxide synthase expression through the inhibition of Janus kinase 2-mediated JNK pathway in lipopolysaccharide-activated murine macrophages", Biochem. Pharmacol, 70, pp.1211~1221 (2005)
- Dommisse, R. A., "Structural analysis of phenolic glucosides from Salicaceae by NMR spectroscopy", Phytochemistry, 25, pp.1201~1204 (1986)
- Deok Sung Bae, "Protopine reduces the inflammatory activity of lipopolysaccharide-stimulated murine macrophages", BMB Reports, 45(2), pp.108~113 (2012), 생화학분자생물학회
- 윤기수, "Curcumin ameliorates TNF-α-induced ICAM-1 expression and subsequent THP-1 adhesiveness via the induction of heme oxygenase-1 in the HaCaT cells", BMB Reports, 46(8), pp.410~415 (2013), 생화학분자생물학회
- 박민철, "CD83 expression induced by CpG-DNA stimulation in a macrophage cell line RAW 264.7", BMB Reports, 46(9), pp.448~453 (2013), 생화학분자생물학회
- 신순영, "Egr-1 regulates the transcription of the BRCA1 gene by etoposide", BMB Reports, 46(2), pp.92~96 (2013), 생화학분자생물학회