The induction of cyclooxygenase-2 elicited by endotoxin in endothelial cells and macrophages is inhibited by prostaglandin E1 and 13,14-dihydro prostaglandin E1.

P Akarasereenont, E Hide, P Ney, C Thiemermann, J R Vane
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引用次数: 5

Abstract

The effects of PGE1 or 13,14-dihydro PGE1 (PGE0) on the expression of COX-2 protein and COX activity elicited by LPS (1 microgram/ml for 24 h) in bovine aortic endothelial cells (BAEC) and J774.2 macrophages were investigated. PGE1 or PGE0 (0.001 to 10 micrograms/ml) caused a dose-dependent decrease of COX activity elicited by LPS in both cell types. Western blot analysis showed that PGE1 or PGE0 (1 microgram/ml) inhibited the expression of COX-2 protein in LPS-activated BAEC and J774.2 macrophages. Thus, PGE1 or (its metabolite) PGE0 decrease the formation of COX metabolites by inhibiting the induction of COX-2 protein by LPS.

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前列腺素E1和13,14-二氢前列腺素E1可抑制内毒素诱导的内皮细胞和巨噬细胞环氧化酶-2的表达。
研究了PGE1或13,14-二氢PGE1 (PGE0)对LPS(1微克/毫升,作用24 h)诱导的牛主动脉内皮细胞(BAEC)和巨噬细胞(J774.2)中COX-2蛋白表达和COX活性的影响。PGE1或PGE0(0.001至10微克/毫升)在两种细胞类型中引起LPS引起的COX活性的剂量依赖性降低。Western blot分析显示,PGE1或PGE0(1微克/ml)可抑制lps活化的BAEC和J774.2巨噬细胞中COX-2蛋白的表达。因此,PGE1或(其代谢物)PGE0通过抑制LPS对COX-2蛋白的诱导而减少COX代谢物的形成。
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