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Anti-inflammatory Activities of GyejigaChulBuTang on Lipopolysaccharide-stimulated RAW264.7 Cells

이승연|강경화|유선애|정민정
대한한방소아과학회 (The Association of Pediatrics of Korean Medicine)|2014.08|대한한방소아과학회지 (The Journal of Pediatrics of Korean Medicine)|제28권 제3호|pp. 47-58|DOI http://dx.doi.org/10.7778/jpkm.2014.28.3.047

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참고문헌

키워드

RAW264.7 cellsInflammationJuvenile rheumatoid arthritisGyejigaChulBuTangProinflammatory cytokine
주제분류한의학

초록

ObjectivesGyejigaChulBuTang (GCBT) is a prescription used to treat acute and chronic arthritis in Korea, China, andJapan. This study assessed the anti-inflammatory and anti-oxidant activities of GCBT on lipopolysaccharide(LPS)-stimulated RAW264.7 macrophage cells. MethodsRaw264.7 cells were pretreated with or without GCBT for 1 hour prior to incubation with LPS. Anti-inflammatory activity of GCBT was evaluated with reference to gene expression and production levels ofproinflammatory cytokines (TNFα, IL-1β, IL-6, GM-CSF and INFγ) and inflammatory mediators (iNOS, COX-2,NO and PGE2). In addition, intracellular ROS generation and signal transduction of MAPK family, PI3K/Akt andIκBα/NFκB was investigated. ResultsPrior treatment with GCBT inhibited elevation of TNFα, IL-1β, IL-6, GM-CSF, INFγ, NO and PGE2, togetherwith their cognate mRNAs in a dose-dependent manner. Intracellular ROS contents were similarly reduced. Theseeffects were due to inhibition of LPS-induced phosphorylation of MAPK family, PI3K/Akt and IκBα as well asnuclear translocation of NFκB. ConclusionsGCBT suppresses pro-inflammatory mediators. GCBT has potential in the treatment of juvenile rheumatoidarthritis associated with inflammation.

Abstract

ObjectivesGyejigaChulBuTang (GCBT) is a prescription used to treat acute and chronic arthritis in Korea, China, andJapan. This study assessed the anti-inflammatory and anti-oxidant activities of GCBT on lipopolysaccharide(LPS)-stimulated RAW264.7 macrophage cells. MethodsRaw264.7 cells were pretreated with or without GCBT for 1 hour prior to incubation with LPS. Anti-inflammatory activity of GCBT was evaluated with reference to gene expression and production levels ofproinflammatory cytokines (TNFα, IL-1β, IL-6, GM-CSF and INFγ) and inflammatory mediators (iNOS, COX-2,NO and PGE2). In addition, intracellular ROS generation and signal transduction of MAPK family, PI3K/Akt andIκBα/NFκB was investigated. ResultsPrior treatment with GCBT inhibited elevation of TNFα, IL-1β, IL-6, GM-CSF, INFγ, NO and PGE2, togetherwith their cognate mRNAs in a dose-dependent manner. Intracellular ROS contents were similarly reduced. Theseeffects were due to inhibition of LPS-induced phosphorylation of MAPK family, PI3K/Akt and IκBα as well asnuclear translocation of NFκB. ConclusionsGCBT suppresses pro-inflammatory mediators. GCBT has potential in the treatment of juvenile rheumatoidarthritis associated with inflammation.

참고문헌 (41)

  1. 김동수, "소아기 류마티스 관절염", Korean Journal of Pediatrics, 50(12), pp.1173~1179 (2007), 대한소아과학회
  2. Phelan JD, "Genomic progress in pediatric arthritis : recent work and future goals", Curr Opin Rheumatol, 18(5), pp.482~489 (2006)
  3. Førre O, "Genetic epidemiology of juvenile idiopathic arthritis", Scand J Rheumatol, 31(3), pp.123~128 (2002)
  4. Murray K, "Pathogenesis of juvenile chronic arthritis : genetic and environmental factors", Arch Dis Child, 77(6), pp.530~534 (1997)
  5. Brewer EJ Jr, "Current proposed revision of JRA criteria. JRA Criteria Subcommittee of the Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Section of The Arthritis Foundation", Arthritis Rheum, 20(2), pp.195~199 (1997)
  6. De Benedetti F, "Is systemic juvenile rheumatoid arthritis an interleukin 6 mediated disease?", J Rheumatol, 25(2), pp.203~207 (1998)
  7. De Benedetti F, "Serum soluble interleukin 6(IL-6)receptor and IL-6", soluble IL-6 receptor complex in systemic juvenile rheumatoid arthritis, 1994, pp.93(5), 2114~2119
  8. Woo P, "The cytokine network in juvenile chronic arthritis", Rheum Dis Clin North Am, 23(3), pp.491~498 (1997)
  9. Morimoto C, "Autoantibody to an immunoregulatory inducer population in patients with juvenile rheumatoid arthritis", J Clin Invest, 67(3), pp.753~761 (1981)
  10. Mangge H, "Serum cytokines in juvenile rheumatoid arthritis. Correlation with conventional inflammation parameters and clinical subtypes", Arthritis Rheum, 38(2), pp.211~220 (1995)
  11. 한윤수, "Pathogenesis and clinical manifestations of juvenile rheumatoid arthritis", Korean Journal of Pediatrics, 53(11), pp.921~930 (2010), 대한소아과학회
  12. Choi J, "A clinical study of juvenile rheumatoid arthritis", J Oriental Rehab Med, 18(2), pp.306~317 (1998)
  13. The korean academy of oriental rehabilitation medicine, "Oriental rehabilitation medicine", pp.78~99 (2005), Koonja
  14. Kaplanski G, "IL-6 : a regulator of the transition from neutrophil to monocyte recruitment during inflammation", Trends Immunol, 24(1), pp.25~29 (2003)
  15. Williams RO, "Anti-tumor necrosis factor ameliorates joint disease in murine collagen-induced arthritis", Proc Natl Acad Sci USA, 89(20), pp.9784~9788 (1992)
  16. Feldmann M, "Rheumatoid Arthritis", Cell, 85, pp.307~310 (1996)
  17. Hom JT, "In vivo administration with IL-1 accelerates the development of collagen-induced arthritis in mice", J Immunol, 141(3), pp.834~841 (1988)
  18. Grom AA, "Patterns of expression of tumor necrosis factor alpha, tumor necrosis factor beta, and their receptors in synovia of patients with juvenile rheumatoid arthritis and juvenile spondylarthropathy", Arthritis Rheum, 39(10), pp.1703~1710 (1996)
  19. Kutukculer N, "Study of pro-inflammatory(TNF-alpha, IL-1alpha, IL-6)and T-cell-derived(IL-2, IL-4)cytokines in plasma and synovial fluid of patients with juvenile chronic arthritis : correlations with clinical and laboratory parameters", Clin Rheumatol, 17(4), pp.288~292 (1998)
  20. Shingu M, "The effects of cytokines on metalloproteinase inhibitors(TIMP)and collagenase production by human chondrocytes and TIMP production by synovial cells and endothelial cells", Clin Exp Immunol, 94(1), pp.145~149 (1993)
  21. Pascual V, "Role of interleukin-1 (IL-1) in the pathogenesis of systemic onset juvenile idiopathic arthritis and clinical response to IL-1 blockade", J Exp Med, 201(9), pp.1479~1486 (2005)
  22. Nishimoto N, "Interleukin 6 : from bench to bedside", Nat Clin Pract Rheumatol, 2(11), pp.619~626 (2006)
  23. Ou LS, "Association between serum inflammatory cytokines and disease activity in juvenile idiopathic arthritis", Clin Rheumatol, 21(1), pp.52~56 (2002)
  24. De Benedetti F, "Correlation of serum interleukin-6 levels with joint involvement and thrombocytosis in systemic juvenile rheumatoid arthritis", Arthritis Rheum, 34(9), pp.1158~1163 (1991)
  25. De Benedetti F, "Differences in synovial fluid cytokine levels between juvenile and adult rheumatoid arthritis", J Rheumatol, 24(7), pp.1403~1409 (1997)
  26. Wallace JL, "Nitric oxide as a regulator of inflammatory processes", Mem Inst Oswaldo Cruz, 100(1), pp.5~9 (2005)
  27. Tinker AC, "Selective inhibitors of inducible nitric oxide synthase: potential agents for the treatment of inflammatory diseases?", Curr Top Med Chem, 6(2), pp.77~92 (2006)
  28. Vane JR, "Inducible isoforms of cyclooxygenase and nitric-oxide synthase in inflammation", Proc Natl Acad Sci USA, 91(6), pp.2046~2050 (1994)
  29. Hla T, "Cyclooxygenase gene expression in inflammation and angiogenesis", Ann NY Acad Sci, 696, pp.197~204 (1993)
  30. Dubois RN, "Cyclooxygenase in biology and disease", FASEB J, 12(12), pp.1063~1073 (1998)
  31. Liang YC, "Suppression of inducible cyclooxygenase and inducible nitric oxide synthase by apigenin and related flavonoids in mouse macrophages", Carcinogenesis, 20(10), pp.1945~1952 (1999)
  32. Floyd RA., "Neuroinflammatory processes are important in neurodegenerative diseases: an hypothesis to explain the increased formation of reactive oxygen and nitrogen species as major factors involved in neurodegenerative disease development", Free Radic Biol Med, 26(9), pp.1346~1355 (1999)
  33. Cesaratto L, "The importance of redox state in liver damage", Ann Hepatol, 3(3), pp.86~92 (2004)
  34. Kabe Y, "Redox regulation of NF-kappaB activation: distinct redox regulation between the cytoplasm and the nucleus", Antioxid Redox Signal, 7(3), pp.395~403 (2005)
  35. Zhang W, "MAPK signal pathways in the regulation of cell proliferation in mammalian cells", Cell Res, 12(1), pp.9~18 (2002)
  36. Silva JD, "Blockade of p38 mitogen-activated protein kinase pathway inhibits inducible nitric-oxide synthase expression in mouse astrocytes", J Biol Chem, 272(45), pp.28373~28380 (1997)
  37. Murphy GM, "Macrophage colony-stimulating factor augments β-amyloid-induced interleukin-1, interleukin-6, and nitric oxide production by microglial cells", J Biol Chem, 273(33), pp.20967~20971 (1998)
  38. Xu X, "p38 MAPK, but not p42", p44 MAPK mediated inducible nitric oxide synthase expression in C6 glioma cells, 2000, pp.67(26), 3221~3230
  39. Fiebich BL, "Inhibition of LPS-induced p42", 44 MAP kinase activation and iNOS, J Neuroimmunol, pp.2002, 132(1)[DOI]
  40. Christman JW, "Redox regulation of nuclear factor kappa B : therapeutic potential for attenuating inflammatory responses", Brain Pathol Zurich Switz, 10(1), pp.153~162 (2002)
  41. Dauphinee SM, "Lipopolysaccharide signaling in endothelial cells", Lab Invest, 86(1), pp.9~22 (2005)

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