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首页> 外文期刊>Osteoarthritis and cartilage >Participation of cyclooxygenase-1 in prostaglandin E2 release from synovitis tissue in primary osteoarthritis in vitro.
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Participation of cyclooxygenase-1 in prostaglandin E2 release from synovitis tissue in primary osteoarthritis in vitro.

机译：体外原发性骨关节炎滑膜组织中环氧化酶-1参与前列腺素E2的释放。

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OBJECTIVES: To investigate the relative contribution of the cyclooxygenase (COX) isoenzymes COX-1 and COX-2 to prostaglandin E2 (PGE2) release from inflamed synovial tissue in N=10 patients with primary osteoarthritis (OA) in vitro and to determine possible effects of COX inhibitors on the gene expression of synovial COX-1 and COX-2. DESIGN: The effects of a COX-unspecific nonsteroidal anti-inflammatory drug (NSAID; diclofenac), a selective COX-1 inhibitor (SC-560) and a selective COX-2 inhibitor (SC-58125) on PGE2 release from inflamed synovial tissue (0.1-10 microM, 3 and 6 h incubation time) were compared. Release of PGE2 into the incubation media was measured by means of the enzyme-linked immunosorbent assay. Expression of synovial COX-1/-2 was quantified by means of real-time reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: All agents inhibited synovial PGE2 release dose-dependently. Compared to short-term incubations, the inhibitory potency of diclofenac, SC-58125 and SC-560 wasincreased (0.1-10 microM) and decreased (0.1-1 microM), respectively, during 6 h: At 10 microM, SC-560 and SC-58125 had obviously lost their specificity for COX-1 and COX-2, respectively, indicated by a comparable inhibitory potency of the selective COX-1 inhibitor (86.6%) and the selective COX-2 inhibitor (96.6%) within identical tissue specimens. In contrast, at 1 microM, 83% and 62.8% inhibition was seen for diclofenac and SC-58125, respectively. SC-560 showed 30.6% inhibition (P<0.05). In contrast to synovial COX-1, RT-PCR revealed a significant induction of COX-2 through PGE2. CONCLUSIONS: With respect to the concentrations studied, the data suggest that in inflamed synovial tissue in OA, up to 30% of PGE2 might be generated via the COX-1 pathway. In therapy of OA, the relative contribution of COX-1 in synovial inflammation should be considered, weighing the potency of COX-unspecific NSAID against the assumed superior gastrointestinal safety profile of selective COX-2 inhibitors.
机译：目的：调查N = 10原发性骨关节炎（OA）患者滑膜组织中环氧合酶（COX）同工酶COX-1和COX-2对前列腺素E2（PGE2）释放的相对贡献，并确定可能的作用抑制剂对滑膜COX-1和COX-2基因表达的影响设计：COX非特异性非甾体抗炎药（NSAID;双氯芬酸），选择性COX-1抑制剂（SC-560）和选择性COX-2抑制剂（SC-58125）对发炎的滑膜组织释放PGE2的影响比较（0.1-10 microM，孵育3和6 h）。通过酶联免疫吸附测定法测量PGE 2释放到培养培养基中。滑膜COX-1 / -2的表达通过实时逆转录聚合酶链反应（RT-PCR）进行定量。结果：所有药物均能剂量依赖性地抑制滑膜PGE2的释放。与短期孵育相比，双氯芬酸，SC-58125和SC-560的抑制力在6小时内分别增加（0.1-10 microM）和降低（0.1-1 microM）：在10 microM时，SC-560和SC-560 SC-58125明显丧失了对COX-1和COX-2的特异性，这在相同组织中具有选择性的COX-1抑制剂（86.6％）和选择性COX-2抑制剂（96.6％）相当的抑制力表明标本。相反，在1 microM时，双氯芬酸和SC-58125的抑制作用分别为83％和62.8％。 SC-560显示出30.6％的抑制（P ＜0.05）。与滑膜COX-1相反，RT-PCR显示通过PGE2显着诱导COX-2。结论：关于所研究的浓度，数据表明在OA的滑膜组织发炎中，多达30％的PGE 2可能通过COX-1途径产生。在OA的治疗中，应考虑COX-1在滑膜炎症中的相对贡献，权衡COX-非特异性NSAID的效力与选择性COX-2抑制剂的假定优越的胃肠道安全性。

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