Prostaglandin F2α-Induced Interleukin-8 Production in Human Dental Pulp Cells Is Associated With MEK/ERK Signaling
Prostaglandin F2α-Induced Interleukin-8 Production in Human Dental Pulp Cells Is Associated With MEK/ERK Signaling
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DOI：
10.1016/j.joen.2008.12.023
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发表时间：
2009-04-01
影响因子：
4.2
通讯作者：
Jeng, Jiiang-Huei
中科院分区：
文献类型：
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作者：
Chang, Mei-Chi;Chang, Hsiao-Hua;Jeng, Jiiang-Huei
前列腺素F-2 α（PGF（2 α））和白细胞介素-1 β（IL-1 β）水平在发炎的牙髓中升高。IL-1 β和PGF（2 α）在牙髓炎症发病机制中的作用有待研究。我们发现IL-1 β刺激人牙髓细胞产生PGF（2 α）。IL-1 β和PGF（2 α）（0.5-10 μ mol/L）也诱导牙髓细胞产生IL-8和mRNA表达。阿司匹林抑制IL-1 β诱导的PGF（2 α），但不抑制IL-8的产生。PGF（2 α）诱导的IL-8产生和mRNA表达被U 0126（一种丝裂原活化蛋白激酶激酶[MEK 1/2]抑制剂）抑制，而SQ 22536（一种腺苷酸环化酶抑制剂）增强了这一作用。这些结果表明，IL-1 β诱导的牙髓细胞中IL-8的产生主要不是通过直接激活环氧合酶和PGF（2 α）的产生。PGF（2 α）诱导的IL-8产生可能是通过激活MEK/细胞外信号调节激酶信号传导，而不是通过激活腺苷酸环化酶。IL-1 β和PGF（2 α）可能通过诱导IL-8的产生参与牙髓炎症的发病机制。（J Endod2009;35：508-512）
Prostaglandin F-2alpha (PGF(2 alpha)) and interleukin-1 beta (IL-1 beta) levels are elevated in inflamed dental pulp. The roles of IL-1 beta and PGF(2 alpha) in the pathogenesis of pulpal inflammation await investigation. We found that IL-1 beta stimulated PGF(2 alpha) production of human dental pulp cells. IL-1 beta and PGF(2 alpha) (0.5-10 mu mol/L) also induced IL-8 production and mRNA expression in pulp cells. Aspirin inhibited IL-1 beta-induced PGF(2 alpha) but not IL-8 production. PGF(2 alpha)-induced IL-8 production and mRNA expression were inhibited by U0126 (an inhibitor of mitogen-activated protein kinase kinase [MEK1/2]) inhibitor), whereas SQ22536 (an adenylate cyclase inhibitor) enhanced this event. These results indicate that IL-1 beta-induced IL-8 production in pulp cells is not mainly via direct activation of cyclooxygenase and PGF(2 alpha) generation. PGF(2 alpha)-induced IL-8 production is possibly via activation of MEK/extracellular signal-regulated kinase signaling, but not by activation of adenylate cyclase. IL-1 beta and PGF(2 alpha) might involve the pathogenesis of pulpal inflammation via induction of IL-8 production. (J Endod2009;35:508-512)