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CD40L刺激诱导型环氧合酶表达及普伐他汀的作用(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2006年第3期
页码:
245-248
栏目:
基础研究
出版日期:
2006-06-25

文章信息/Info

Title:
Effect of pravastatin on cyclooxygenase-2 expression induced by rhCD40L in cultured U937 cells
作者:
樊民1吴宗贵1李岚2李洪涛1王磊1潘晓明1
1.第二军医大学长征医院心内科,上海 200003; 2. 上海411医院内四科,上海 200003
Author(s):
FAN Min WU Zong-gui LI Lan Li Hong-tao Wang Lei Pan Xiao-ming
Department of Cardiovasology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
关键词:
CD40配体诱导型环氧合酶普伐他汀单核细胞
Keywords:
CD40 ligandcyclooxygenase-2pravastatinmonocyte
分类号:
Q946.5; R972.9
DOI:
-
文献标识码:
A
摘要:
目的 探讨重组人CD40配体(rhCD40L)对培养的人单核细胞(U937)表达诱导型环氧合酶(COX-2)的作用和普伐他汀对其影响。方法 体外培养U937细胞,以0.05、0.1、0.2 μg/ml的rhCD40L分别刺激24 h;0.4 μg/ml的rhCD40L分别刺激3、6、12、24 h;终浓度10、1、0.1 mmol/L的普伐他汀与0.4μg/ml的rhCD40L共同刺激U937细胞24 h。RT-PCR检测COX-2 mRNA表达,Westernblot 检测COX-2蛋白表达,ELISA法检测前列腺素E2(PGE2)的浓度反映COX-2酶活性。结果 0.4 μg/ml的rhCD40L刺激后3 h可诱导COX-2 mRNA和蛋白表达,随着rhCD40L浓度和作用时间增加,COX-2 mRNA和蛋白表达显著增加(P<0.01),且呈时效和量效关系;同样,rhCD40L以时间和剂量依赖的方式增加U937细胞中PGE2的合成。0.4 μg/ml的rhCD40L与普伐他汀共同刺激24 h后,COX-2的表达显著被抑制。结论 rhCD40L以时间和浓度依赖的方式诱导COX-2的表达,普伐他汀可以抑制此作用。
Abstract:
AIM To evaluate cyclooxygenase2 expression induced by rhCD40L in cultured U937 cells and possible inhabition inhibition by pravastatin. METHODS U937 cells were pretreated with rhCD40L of different concentrations and time intervals and COX2 mRNA and protein expression were observed by RTPCR and Westernblot respectively. For COX2 enzyme activity, PGE2 released by U937 cells was measured by ELISA. RESULTS rhCD40L increased the expression of COX2 in a time and dosedependent manner (P<0.01). Pravastatin inhibited the expression of COX2 induced by rhCD40L in a dosedependent manner (P<0.01). CONCLUSION rhCD40L can induce cyclooxygenase2 expression in a dose and time dependent manner. Pravastatin inhibits this enhanced expression in U937 cells.

参考文献/References

[1] Rose R. Atherosclerosis  an inflammatory disease[J]. N Engl J Med, 1999, 340(2):115-126.

[2] Linton MF, Fazio S. Cyclooxygenase2 and atherosclerosis[J]. Curr Opin Lipidol, 2002,13(5): 497-504.

[3] Mitchell JA, Warner TD. Cyclooxygenase2: pharmacology, physiology, biochemistry and relevance to NSAID therapy[J]. Br J Pharmacol, 1999, 128(6): 1121-1132.

[4] Massy ZA, Swan SK. Cyclooxygenase2 and atherosclerosis: friend or foe?[J]. Nephrol Dial Transplant, 2001, 16(12): 2286-2289.

[5] Aukrust P, Muller F, Ueland T, et al. Enhanced levels of soluble and membranebound CD40 ligand in patients with unstable angina. Possible reflection of T lymphocyte and platelet involvement in the pathogenesis of acute coronary syndromes[J]. Circulation, 1999,100(6):614-620.

[6] Lutgens E, Daemen MJ. CD40CD40L interactions in atherosclerosis[J]. Trends Cardiovasc Med, 2002,12(1):27-32.

[7] Lutgens E, Gorelik L, Daemen MJ, et al. Requirement for CD154 in the progression of atherosclerosis[J]. Nat Med,1999,5(11):1313-1316.

[8] Schonbeck U, Libby P. CD40 signaling and plaque instability[J]. Circ Res, 2001,89(12):1092-1103.

[9] Mach F, Schonbeck U,Bonnefoy JY, et al. Activation of monocyte/macrophage functions related to acute atheroma complication by ligation of CD40: induction of collagenase, stromelysin, and tissue factor[J]. Circulation, 1997,96(2):396-399.

[10]Zhang Y, Cao HJ, Graf B, et al. CD40 engagement upregulates cyclooxygenase2 expression and prostaglandin E2 production in human lung fibroblasts[J]. J Immunol,1998,160(3):1053-1057.

[11]DongariBagtzoglou AI, Thienel U, Yellin MJ. CD40 ligation triggers COX2 expression in endothelial cells: evidence that CD40mediated IL6 synthesis is COX2dependent[J]. Inflamm Res,2003,52(1):18-25.

[12]HernandezPresa MA, MartinVentura JL, Ortego M, et al. Atorvastatin reduces the expression of cyclooxygenase2 in a rabbit model of atherosclerosis and in cultured vascular smooth muscle cells[J]. Atherosclerosis,2002,160(1):49-58.

[13]MartinVentura JL, BlancoColio LM, GomezHernandez A, et al.Intensive treatment with atorvastatin reduces inflammation in mononuclear cells and human atherosclerotic lesions in one month[J]. Stroke, 2005,36(8):1796-800.

[14]Chen JC, Huang KC, Wingerd B, et al.HMGCoA reductase inhibitors induce COX2 gene expression in murine macrophages: role of MAPK cascades and promoter elements for CREB and C/EBPbeta[J]. Exp Cell Res, 2004,301(2):305-319.

备注/Memo

备注/Memo:
收稿日期:2005-09-16.通讯作者:吴宗贵,主任医师,主要从事炎症与动脉粥样硬化研究 作者简介:樊民,主治医师,博士 Tel:(021)6361010973202 Email:fanmin@medmail.com.cn
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