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目的 研究膜相关前列腺素E2 合成酶 (membrane associatedprostagladinE2 synthase ,mPGES)与类风湿关节炎的关系。方法 用反转录聚合酶链反应 (RT PCR) ,酶联免疫吸附测定法 (ELISA)等方法分析环氧化酶 2(cyclooxygenase 2 ,COX 2 ) ,mPGES基因转录和表达以及前列腺素E2 (PGE2 )合成。结果 白细胞介素 (IL) 1β可诱导滑膜成纤维细胞COX 2 ,mPGES转录水平升高 ,主要的炎性介质PGE2 合成增加。COX 2抑制剂NS 398和mPGES抑制剂MK 886可降低IL 1β诱导的PGE2 合成增加。提示COX 2、mPGES、PGE2 三者密切相关。丝裂原激活蛋白激酶(MAPK)抑止剂PD和SB可降低IL 1β诱导的滑膜成纤维细胞COX 2 ,mPGES转录水平。 结论 mPGES可能成为RA防治新的分子靶点
Objective To investigate the relationship between membrane associated prostaglandin E2 synthase (mPGES) and rheumatoid arthritis. Methods The transcription and expression of cyclooxygenase 2 (COX 2), mPGES gene and the expression of prostaglandin E2 (PGE2) were analyzed by reverse transcription polymerase chain reaction (RT PCR) and enzyme linked immunosorbent assay (ELISA) )synthesis. Results Interleukin (IL) 1β induced the transcription of COX 2 and mPGES in synovial fibroblasts and increased the synthesis of PGE2, a major inflammatory mediator. The COX 2 inhibitor NS 398 and the mPGES inhibitor MK 886 reduced the IL 1β-induced increase in PGE 2 synthesis. Tip COX 2, mPGES, PGE2 are closely related to each other. Mitogen-activated protein kinase (MAPK) inhibitors PD and SB decreased IL 1β-induced COX 2 and mPGES transcription in synovial fibroblasts. Conclusion mPGES may be a new molecular target for RA therapy