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p38丝裂原活化蛋白激酶信号级联在炎症反应中的作用 被引量:10

p38 MAPK signalling cascades and inflammatory disease
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摘要 在急、慢性疾病中 ,细胞释放的炎症介质可以活化多种信号转导级联反应 ,丝裂原活化蛋白激酶 (MAPK)信号转导通道在招募白细胞于炎症部位聚集起着重要的作用。同时 ,p38MAPK异构体的活化可以激活致炎细胞因子 ,而后刺激白细胞活化。然而 ,p38MAPK引起的白细胞招募这一系列的功能过程包括 :粘附、游走和效应器的功能如氧化爆发以及 p38MAPK介导的复杂细胞因子网络在炎症中的作用仍有待研究。针对减少炎症介质产生和以 p38MAPK为治疗靶点的研究正在进行中 ,不远的将来可能会成为治疗炎症疾病的新策略。 Inflammatory mediators releasing during acute and chronic diseases can activate multiple intracellular signals inducing cascades of the mitogen-activated protein kinase(MAPK) signalling transduction pathway. MAPK plays a significant role in the recruitment of leukocytes to the inflammation sites. Stimulation of leukocytes by pro-inflammatory cytokines is known to activate the MAPK isoform p38. However, the consequences of p38MAPK activation during leukocyte recruitment, adhesion, migration, functions of effector(oxidative burst), and the network of cytokines mediated by p38MAPK are all investigated for further elucidation. Specific p38 inhibitors in reducing the production of inflammatory mediators and providing more effective treatment are now being developed.
出处 《医学研究生学报》 CAS 2004年第8期737-740,共4页 Journal of Medical Postgraduates
关键词 P38丝裂原活化蛋白激酶 信号转导 炎症反应 p38MAPK Signalling transduction Inflammation
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参考文献21

  • 1[1]Mi-Sun K, Hyun J, Jae-Young U et al. Agonists of proteinase-activated receptor 2 induce TNF-alpha secretion from astrocytoma cells[J]. Cell Biochem Funct, 2002, 20 (4): 339- 345.
  • 2[2]Huang CD, Tliba O, Panettieri RA et al. Bradykinin induces interleukin-6 production in human airway smooth muscle cells: modulation by Th2 cytokines and dexamethasone[J]. Am J Respir Cell Mol Biol, 2003, 28(3): 330-338.
  • 3[3]Yuasa T, Ohno S, Kehrl JH et al. Tumor necrosis factor signaling to stress- activated protein kinase( SAPK)/ Jun- NH2- terminal kinase( JNK) and p38[J]. J Biol Chem, 1998, 273: 22681-22692.
  • 4[4]Hale KK, Trollinger D, Rihanek M et al. Differential expression and activation of p38 mitogen-activated protein kinase α,β,γandδ in inflammatory cell lineages[J]. J Immunol,1999, 162: 4246-4252.
  • 5[5]Chen P, Li J, Barnes J et al. Restraint of proinflammatory cytokine biosynthesis by mitogen- activated protein kinase phosphatase-1 in lipopolysaccharide-stimulated macrophages[J]. J Immunol,2002, 169(11): 6408-1646.
  • 6[6]Deak M, Clifton AD, Lucocq JM et al. Mitogen- and stress-activated protein kinase-1 (MSK1) is directly activated by MAPK and SAPK2/p38, and may mediate activation of CREB[J]. EMBO J, 1998, 17: 4426-4441.
  • 7[7]Wong CK, Ip WK, Lam CW et al. IL-3, 5 and GM- CSF- induced Adhesion Molecule Expression on Eosinophils by p38MAPK and NF-κB[J]. Am J Respir Cell Mol Biol, 2003, 29(1): 133- 147.
  • 8[8]Blaber R, Stylianou E, Clayton A et al. Selective Regulation of ICAM-1 and RANTES Gene Expression after ICAM-1 Ligation on Human Renal Fibroblasts[J]. J Am Soc Nephrol, 2003, 14(1): 116-127.
  • 9[9]Nick JA, Young SK, Arndt PG et al. Selective suppression of neutrophil accumulation in ongoing pulmonary inflammation by systemic inhibition of p38 mitogen-activated protein kinase[J]. J Immunol, 2002, 169(9): 5260-5269.
  • 10[10]You-Li Zu, Jiafan Q, Annette G et al. p38 mitogen-activated protein kinase activation is required for human neutrophil function triggered by TNF-γ or FMLP stimulation[J]. J Immunol, 1998, 160: 1982-1989.

二级参考文献46

  • 1[16]Saldeen J, Lee JC, Welsh N. Role of p38 mitogen activated protein kinase(p38 MAPK) in cytokine-induced islet islet cell apoptosis. Biochem Pharmacol, 2001,61:1561-1569
  • 2[17]Jeon YJ, Han SB, Lee SH, et al. Activation of mitogen activated protein kinase pathways by angelan in murine macrophages. Int Immunopharmacol, 2001,1 : 237-245.
  • 3[18]Chan ED, Riches DW. IFN-gamma + LPS induction of iNOS is modulated by ERK, JNK/SAPK, and p38 MAPK in a mouse macrophage cell line. Am J Physiol Cell Physiol, 2001,280: C441-450.
  • 4[21]Chae HJ, Kim SC, Chae SW, et al. Blockade of the p38mitogen-activated protein kinase pathway inhibits inducible nitric oxide synthase and interleukin-6 expression in MC3T3E-1 osteoblasts. Pharmacol Res, 2001, 43: 275-283.
  • 5[22]Ajizian SJ, English BK, Meals EA. Specific inhibitors of p38 and extracellular-regulated kinase mitogen-activated n kinase pathways block inducible nitric oxide syn thase and tumor necrosis factor accumulation in murinemacrophages stimulated with lipopolysaccharide and inter feron-γ. J Infect Dis, 1999, 179: 939-944.
  • 6[23]Miles PR, Bowman L, Rao KMK, et al. Pulmonary sur factant inhibits LPS-induced nitric oxide production by al veolar macrophages. Am J Physiol, 1999, 276: L186 L196.
  • 7[24]Hori M, Kita M, Torihashi S, et al. Upregulation of iNOS by COX-2 in muscularis resident macrophage of rat intestine stimulated with LPS. Am J Physiol Gastrointest Liver Physiol, 2001,280(5): G930-G938.
  • 8[1]Green LC, WagnerDA, GlogowskiJ, etal. Analysis of ni trate, and [15N] nitrate in biological fluids. Anal Biochem, 1982,126:131-138.
  • 9[2]Luss H, Nussler NC, Beger HG, et al. Expression and de tection of inducible nitric oxide synthase in experimental models of inflammation. Methods, 1996,10:51-60.
  • 10[3]Akaike T, Nogchi Y, Ijiri S, et al. Pathogenesis of influ enza virus-induced pneumonia: involvement of both nitric oxide and oxygen radicals. Proc Natl Acad Sci USA, 1996,93: 2448-2453.

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