首页> 外文期刊>Journal of pharmacological sciences. >Curcumin Inhibits the Proteinase-Activated Receptor-2–Triggered Prostaglandin E2 Production by Suppressing Cyclooxygenase-2 Upregulation and Akt-Dependent Activation of Nuclear Factor-κB in Human Lung Epithelial Cells
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Curcumin Inhibits the Proteinase-Activated Receptor-2–Triggered Prostaglandin E2 Production by Suppressing Cyclooxygenase-2 Upregulation and Akt-Dependent Activation of Nuclear Factor-κB in Human Lung Epithelial Cells

机译:姜黄素抑制人肺上皮细胞中环氧合酶-2的上调和Akt依赖的核因子-κB的活化,从而抑制蛋白酶激活的受体2触发的前列腺素E2的产生。

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References(15) Cited-By(11) We performed this study to determine if curcumin affects pro-inflammatory responses to activation of proteinase-activated receptor-2 (PAR2) in human pulmonary adenocarcinoma A549 cells. Curcumin completely inhibited the PAR2-triggered prostaglandin E2 (PGE2) production, but notably not interleukin-8 release. Cyclooxygenase-2 (COX-2) upregulation, but not its upstream activation of mitogen-activated protein kinases, caused by PAR2 stimulation was partially inhibited by curcumin. Curcumin inhibited the PAR2-triggered phosphorylation of I-κB, an indicator for nuclear factor-κB (NF-κB) activation, and also its upstream signal Akt, which is known to contribute to PAR2-triggered PGE2 formation, but not COX-2 upregulation. Collectively, curcumin inhibits the PAR2-triggered PGE2 production by suppressing COX-2 upregulation and Akt/NF-κB signals in A549 cells.
机译:参考文献(15)Cited-By(11)我们进行了这项研究,以确定姜黄素是否影响人肺腺癌A549细胞中对蛋白酶激活受体2(PAR2)活化的促炎反应。姜黄素完全抑制PAR2触发的前列腺素E2(PGE2)的产生,但不明显抑制白介素8的释放。姜黄素可部分抑制由PAR2刺激引起的环氧合酶2(COX-2)的上调,但对上游的丝裂原活化蛋白激酶的上游激活不起作用。姜黄素抑制PAR2触发的I-κB磷酸化,I-κB是核因子-κB(NF-κB)活化的指示剂,并且还抑制其上游信号Akt,已知它有助于PAR2触发的PGE2形成,但对COX-2无效。上调。姜黄素通过抑制A549细胞中的COX-2上调和Akt /NF-κB信号共同抑制PAR2触发的PGE2的产生。

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