地塞米松通过诱导环氧化酶1使NG108 - 15细胞分化。

Dexamethasone differentiates NG108-15 cells through cyclooxygenase 1 induction.

作者信息

Kim Hyeon Soo, Song Minseok, Kim Euikyung, Ryu Sung Ho, Suh Pann-Ghill

机构信息

Department of Life Science, Division of Molecular and Life Science, Pohang University of Science and Technology, San 31 Hyoja-dong, Nam-gu, Pohang, Kyungbuk 790-784, Korea.

出版信息

Exp Mol Med. 2003 Jun 30;35(3):203-10. doi: 10.1038/emm.2003.28.

DOI:10.1038/emm.2003.28

PMID:12858020

Abstract

Cyclooxygenase (COX) is a key enzyme in the conversion of arachidonic acid into prostanoids which participate in various cellular functions including apoptosis, mitogenesis, inflammation, immune modulation and differentiation. Moreover, the synthetic glucocorticoid, dexamethasone has immune modulating and anti-inflammatory effects in vivo. Recently, dexamethasone was found to enhance retinoic acid-induced neuronal differentiation. In this study, we investigated the mechanisms of dexamethasone-mediated neuronal differentiation. Immunoblotting and morphological analysis demonstrated that dexamethasone induced neuronal differentiation through COX 1 induction. This phenomenon was inhibited by indomethacin, a COX inhibitor. In addition, the addition of exogenous prostaglandin E2 (PGE2), a substance produced by the COX-mediated pathway, triggered neurite outgrowth of cells treated with COX inhibitor. Taken together, COX 1 appears to play an important role in dexamethasone-mediated neuronal differentiation.

摘要

环氧化酶（COX）是将花生四烯酸转化为前列腺素的关键酶，前列腺素参与多种细胞功能，包括细胞凋亡、有丝分裂、炎症、免疫调节和分化。此外，合成糖皮质激素地塞米松在体内具有免疫调节和抗炎作用。最近，发现地塞米松可增强视黄酸诱导的神经元分化。在本研究中，我们研究了地塞米松介导的神经元分化机制。免疫印迹和形态学分析表明，地塞米松通过诱导COX 1来诱导神经元分化。这种现象被COX抑制剂吲哚美辛所抑制。此外，添加外源性前列腺素E2（PGE2），一种由COX介导途径产生的物质，可触发用COX抑制剂处理的细胞的神经突生长。综上所述，COX 1似乎在地塞米松介导的神经元分化中起重要作用。