前列腺素E2与肿瘤坏死因子-α在类风湿性关节炎中的关系及药物的调控作用

中国临床药理学与治疗学 ›› 2011, Vol. 16 ›› Issue (8): 951-955.

前列腺素E₂与肿瘤坏死因子-α在类风湿性关节炎中的关系及药物的调控作用

张磊¹, 魏伟²

¹安徽医科大学第四附属医院药剂科,合肥 230022, 安徽;
²安徽医科大学临床药理研究所,合肥 230022,安徽

收稿日期:2011-04-26 修回日期:2011-08-05 出版日期:2011-08-26 发布日期:2011-09-07
通讯作者: 魏伟, 男,博士,教授,博士生导师,研究方向: 抗炎免疫药理学。E-mail: wwei@ahmu.edu.cn
作者简介:张磊, 男,硕士,研究方向:抗炎免疫药理学。Tel: 0551-2879524 E-mail: zhanglen109@sina.com
基金资助:
安徽医科大学校科研基金(2011xkj091)

Relationship between PGE₂,its correlation factors and TNF-α in rheumatoid arthritis and the regulation of drug

ZHANG Lei¹, WEI Wei²

¹Pharmacy of the Fourth Affiliated Hospital of Anhui Medical University, Hefei 230022,Anhui, China;
²Institute of Clinical Pharmacology, Anhui Medical University, Hefei 230022,Anhui, China

Received:2011-04-26 Revised:2011-08-05 Online:2011-08-26 Published:2011-09-07

摘要/Abstract

摘要： 类风湿性关节炎(RA)是一种常见的慢性、系统性自身免疫疾病。TNF-α与前列腺素E₂(PGE₂)是RA发病过程中的重要炎性介质。已知大量的药物在治疗RA中有效,但是很多药物只能简单地发挥抗炎作用而不能从机理上解决问题,同时还产生一些严重的并发症。本文就PGE₂及其相关细胞因子与TNF-α在RA中的关系以及药物的调控作用研究作一简要概述。

关键词: 类风湿性关节炎, TNF-α, PGE₂

Abstract: Rheumatoid arthritis(RA) is a common chronic, inflammatory, systematic autoimmunity disease.Tumor necrosis factor (TNF-α) and prostaglandin E₂ (PGE₂) are major inflammatory mediators in RA.A lot of compounds are available to treat RA,but most of anti-rheumatic drugs only stay in controlling inflammation symptom and can't modify the progression of the disease, simultaneously accompany with severe side adverse effect.The article reviews the relationship between PGE₂,its correlation factors and TNF-α in rheumatoid arthritis and the therapeutic effect of drugs on RA.

Key words: Rheumatoid arthritis, Tumor necrosis factor alpha, Prostaglandin E₂

中图分类号:

R593.22

张磊, 魏伟. 前列腺素E₂与肿瘤坏死因子-α在类风湿性关节炎中的关系及药物的调控作用[J]. 中国临床药理学与治疗学, 2011, 16(8): 951-955.

ZHANG Lei, WEI Wei. Relationship between PGE₂,its correlation factors and TNF-α in rheumatoid arthritis and the regulation of drug[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2011, 16(8): 951-955.

参考文献

[1] Lemieux LI, Rahal SS,J Kennedy CR.PGE₂ reduces arachidonic acid release in murine podocytes: evidence for an autocrine feedback loop[J].Am J Physiol Cell Physiol, 2003, 284(2): C302-309.
[2] 孙铁铮,吕厚山.IL-1β和TNF-α诱导RA成纤维样滑膜细胞ICAM-1和VCAM-1表达调控的机制研究[J].中华风湿病学杂志, 2005, 9(3): 133-137.
[3] Manicourt DH, Poilvache P.Synovial fluid levels of tumor necrosis factor alpha and oncostatin M correlate with levels of markers of the degradation of crosslinked collagen and cartilage aggrecan in rheumatoid arthritis but not in osteoarthritis[J].Arthritis Rheum,2000,43(2):281-288.
[4] Akaogi J, Nozaki T, Satoh M, et al.Role of PGE₂ and EP receptors in the pathogenesis of rheumatoid arthritis and as a novel therapeutic strategy[J].Endocr Metab Immune Disord Drug Targets,2006,6(4):383-394.
[5] Yamane H, Sugimoto Y, Tanaka S, et al. Prostaglandin E(2) receptors, EP2 and EP4, differentially modulate TNF-alpha and IL-6 production induced by lipopolysaccharide in mouse peritoneal neutrophils[J]. Biochem Biophys Res Commun, 2000, 278(1):224-228.
[6] Treffkorn L, Scheibe R, Maruyama T, et al. PGE₂ exerts its effect on the LPS-induced release of TNF-alpha, ET-1, IL-1alpha, IL-6 and IL-10 via the EP2 and EP4 receptor in rat liver macrophages[J]. Prostaglandins Other Lipid Mediat, 2004, 74(1/2/3/4):113-123.
[7] Shinomiya S, Naraba H, Ueno A, et al.Regulation of TNFalpha and interleukin-10 production by prostaglandins I(2) and E(2): studies with prostaglandin receptor-deficient mice and prostaglandin E-receptor subtype-selective synthetic agonists[J]. Biochem Pharmacol, 2001, 61(9):1153-1160.
[8] 张磊,魏伟,常艳,等.TNF-α对胶原性关节炎大鼠滑膜细胞功能的影响及白芍总苷的作用[J].中国新药杂志,2007,16(7):519-522.
[9] Chang Y, Wei W, Zhang L, et al. Effects and mechanisms of total glucosides of paeony on synoviocytes activities in rat collagen-induced arthritis[J].J Ethnopharmacol,2009,121(1):43-48.
[10] Takasugi K, Yamamura M, Iwahashi M, et al. Induction of tumour necrosis factor receptor-expressing macrophages by interleukin-10 and macrophage colony-stimulating factor in rheumatoid arthritis[J].Arthritis Res Ther,2006,8(4):R126.
[11] Ebrahimi AA, Noshad H, Sadreddini S, et al. Serum levels of TNF-alpha, TNF-alphaRI, TNF-alphaRII and IL-12 in treated rheumatoid arthritis patients[J]. Iran J Immunol,2009, 6(3):147-153.
[12] Smith WL, DeWitt DL, Garavito RM. Cyclooxygenases: structural, cellular, and molecular biology[R]. Annu Rev Biochem, 2000, 69:145-182.
[13] Hinz B, Brune K. Cyclooxygenase-2--10 years later[J]. J Pharmacol Exp Ther, 2002, 300(2): 367-375.
[14] Bachar O, Rose AC, Adner M, et al. TNF alpha reduces tachykinin, PGE₂-dependent, relaxation of the cultured mouse trachea by increasing the activity of COX-2[J]. Br J Pharmacol, 2005, 144(2):220-230.
[15] Pettus BJ, Bielawski J, Porcelli AM, et al.The sphingosine kinase 1/sphingosine-1-phosphate pathway mediates COX-2 induction and PGE₂ production in response to TNF-alpha[J]. FASEB J, 2003, 17(11):1411-1421.
[16] McCoy JM, Wicks JR,Audoly LP. The role of prostaglandin E₂ receptors in the pathogenesis of rheumatoid arthritis[J]. J Clin Invest, 2002, 110(5): 651-658.
[17] Murakami M, Nakashima K, Kamei D, et al. Cellular prostaglandin E₂ production by membrane-bound prostaglandin E synthase-2 via both cyclooxygenases-1 and -2[J]. J Biol Chem,2003, 278(39):37937-37947.
[18] Fahmi H. mPGES-1 as a novel target for arthritis[J]. 2004,16(5):623-627.
[19] Ivanov AI, Romanovsky AA.Prostaglandin E₂ as a mediator of fever: synthesis and catabolism[J]. Front Biosci,2004, 9:1977-1993.
[20] Uracz W, Uracz D, Olszanecki R, et al. Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells[J]. J Physiol Pharmacol,2002, 53(4Pt1):643-654.
[21] Han R, Tsui S, Smith TJ.Up-regulation of prostaglandin E₂ synthesis by interleukin-1beta in human orbital fibroblasts involves coordinate induction ofprostaglandin-endoperoxide H synthase-2 and glutathione-dependent prostaglandin E₂ synthase expression[J]. J Biol Chem, 2002, 277(19):16355-16364.
[22] Kojima F, Naraba H, Sasaki Y, et al. Prostaglandin E₂ is an enhancer of interleukin-1beta-induced expression of membrane-associated prostaglandin E synthase in rheumatoid synovial fibroblasts[J]. Arthritis Rheum,2003, 48(10):2819-2828.
[23] Saegusa M, Murakami M, Nakatani Y, et al. Contribution of membraneassociated prostaglandin E₂ synthase to bone resorption[J]. J Cell Physiol,2003, 197(3):348-356.
[24] Murakami M, Naraba H, Tanioka T, et al. Regulation of prostaglandin E₂ biosynthesis by inducible membrane-associated prostaglandin E₂ synthase that acts in concert with cyclooxygenase-2[J]. J Biol Chem,2000, 275(42):32783-32792.
[25] Matsuno H, Yudoh K, Katayama R, et al. The role of TNF-alpha in the pathogenesis of inflammation and joint destruction in rheumatoid arthritis (RA): a study using a human RA/SCID mouse chimera[J].Rheumatology (Oxford),2002,41(3):329-337.
[26] Noguchi K, Maeda M, Ruwanpura SM, et al. Prostaglandin E₂ (PGE₂) downregulates interleukin (IL)-1alpha-induced IL-6 production via EP2/EP4 subtypes of PGE₂ receptors in human periodontal ligament cells[J].Oral Dis,2005, 11(3):157-162.
[27] 常艳,魏伟,张磊,等. 白芍总苷对IL-1α诱导胶原性关节炎大鼠成纤维样滑膜细胞功能的影响[J].中国药理学通报,2007,23(2):185-188.
[28] 沈玉先,魏伟,徐叔云. 白芍总苷的药理作用及机制[M] //吴曙光,张洪泉,魏伟等主编. 抗炎免疫药理学进展. 上海:第二军医大学出版社,2001:162-167.
[29] 戴敏,魏伟,汪倪萍,等. 木瓜苷对大鼠佐剂性关节炎的治疗作用[J].中国药理学通报,2003,19(3):340-344.
[30] Xu HM, Wei W, Jia XY, et al.Effects and mechanisms of total glucosides of paeony on adjuvant arthritis in rats [J].J Ethnopharmacol,2007,109(3):442-448.
[31] Nam KW, Je KH, Lee JH, et al. Inhibition of COX-2 activity and proinflammatory cytokines (TNF-alpha and IL-1beta) production by water-soluble sub-fractionated parts from bee (Apis mellifera) venom[J]. Arch Pharm Res, 2003, 26(5):383-388.
[32] Kim BH, Kang KS, Lee YS. Effect of retinoids on LPS-induced COX-2 expression and COX-2 associated PGE(2) release from mouse peritoneal macrophages and TNF-alpha release from rat peripheral blood mononuclear cells[J].Toxicol Lett, 2004, 150(2):191-201.
[33] Güler-Yüksel M, Allaart CF, Watt I, et al. Treatment with TNF-α inhibitor infliximab might reduce hand osteoarthritis in patients with rheumatoid arthritis[J].Osteoarthritis Cartilage,2010,18(10):1256-1262.
[34] Jin J, Chang Y, Wei W. Clinical application and evaluation of anti-TNF-alpha agents for the treatment of rheumatoid arthritis[J].Acta Pharmacol Sin,2010,31(9):1133-1140.

前列腺素E₂与肿瘤坏死因子-α在类风湿性关节炎中的关系及药物的调控作用

Relationship between PGE₂,its correlation factors and TNF-α in rheumatoid arthritis and the regulation of drug

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