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系统性红斑狼疮患者外周血单个核细胞环氧合酶同工酶mRNA的表达 被引量:5

Expression of cyclooxygenase isozyme mRNA in the peripheral blood mononuclear cells of patients with systemic lupus erythematosus
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摘要 目的 探讨原生型环氧合酶 (COX 1)和诱生型环氧合酶 (COX 2 )在系统性红斑狼疮(SLE)患者外周血单个核细胞 (PBMC)中的表达水平及其在SLE发病机制中的作用及其意义。方法 应用逆转录 聚合酶链反应 (RT PCR)检测了 34例活动期SLE患者和 30名正常人PBMC中COX 1和COX 2mRNA的表达水平。结果 活动期SLE患者COX 1和COX 2的阳性表达率与正常对照组相比差异无显著性 (P >0 0 5 ) ;活动期SLE患者PBMC中COX 2mRNA的平均表达水平 (0 6 6±0 2 7)明显高于正常对照组 (0 43± 0 16 ) ,差异有非常显著性 (P <0 0 1) ;活动期SLE组COX 1的平均表达水平与正常对照组处于同一表达水平 ,差异性无统计学意义 (P >0 0 5 )。结论 活动期SLE患者外周血单个核细胞中COX 2mRNA的表达增加 ,通过诱导前列腺素 (PGs)的产生参与SLE的发病过程。为特异性COX 2抑制剂应用于SLE的治疗提供了理论依据。 Objective To investigate the roles of constitutive cyclooxygenase (COX 1) and inducible cyclooxygenase (COX 2) expression in the pathogenesis of systemic lupus erythematosus (SLE) and their significance.Method Applying reverse transcription polymerase chain reaction (RT PCR) technique to semiquantitatively analyze COX 1 and COX 2 mRNA expression in the peripheral blood mononuclear cells (PBMC) from 34 active SLE patients and 30 healthy subjects.Results Compared with normal controls,there were no statistical differences in the positive rates of COX 1 and COX 2 expression in SLE patients in active stage ( P >0 05,both).The mean level of COX 2 mRNA expression in active SLE group was significantly higher than that in normal controls ( P <0 01),however there was no significant difference in the mean level of COX 1 mRNA expression between patients with active SLE and normal controls ( P >0 05).Conclusion The level of COX 2 mRNA expression in active SLE group is markedly increased,which may be involved in the pathogenesis of SLE and provides a valuable scientific basis on the clinical use of specific COX 2 inhibitors.
出处 《中华风湿病学杂志》 CAS CSCD 2001年第5期292-294,共3页 Chinese Journal of Rheumatology
基金 卫生部科研基金资助项目 ( 98 1 0 41)
关键词 系统性红斑狼疮 前列腺素内过氧化物合酶 单核白细胞 SLE mRNA COX-1 COX-2 PBMC Lupus erythematosus,systemic Prostaglandin endoperoxide synthetase Leukocytes,mononuclear
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  • 1Tao X,Arthritis Rheum,1998年,41卷,130页

同被引文献29

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