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COX inhibitors downregulate PDE4D expression in a clinical model of inflammatory pain.

机译:Cox抑制剂在炎症疼痛的临床模型中下调PDE4D表达。

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Tumor necrosis factor-alpha (TNF-alpha) has a central role in inflammation and is modulated by prostaglandin E(2) (PGE(2)) and cyclic adenosine monophosphate (cAMP). Using microarray, quantitative real-time polymerase chain reaction (qRT-PCR), and protein detection techniques, we showed that ketorolac and rofecoxib had no significant effect on TNF-alpha gene expression in oral mucosal biopsies 3 h after surgery. They both, however, downregulated the gene and protein expression of phosphodiesterase type 4 (PDE4D), which might represent a novel mechanism contributing to their analgesic and anti-inflammatory effects.
机译:肿瘤坏死因子-α(TNF-α)在炎症中具有核心作用,并通过前列腺素E(2)(PGE(2))和环状腺苷一磷酸(CAMP)调节。 使用微阵列,定量实时聚合酶链反应(QRT-PCR)和蛋白质检测技术,我们显示Ketorolac和Rofecoxib对手术后3小时的口腔粘膜活组织检查中的TNF-α基因表达没有显着影响。 然而,它们都是下调磷酸二酯酶类型4(PDE4D)的基因和蛋白表达,这可能代表一种有助于其镇痛和抗炎作用的新机制。

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