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姜黄素通过抑制BV2小胶质细胞中的激活蛋白1和核因子κB结合来抑制脂多糖诱导的环氧化酶-2表达。

Curcumin suppresses lipopolysaccharide-induced cyclooxygenase-2 expression by inhibiting activator protein 1 and nuclear factor kappab bindings in BV2 microglial cells.

作者信息

Kang Gu, Kong Pil-Jae, Yuh Young-Jin, Lim So-Young, Yim Sung-Vin, Chun Wanjoo, Kim Sung-Soo

机构信息

Department of Pathology, College of Medicine, Kangwon National University, Chunchon, South Korea.

出版信息

J Pharmacol Sci. 2004 Mar;94(3):325-8. doi: 10.1254/jphs.94.325.

DOI:10.1254/jphs.94.325
PMID:15037818
Abstract

Inflammation is a significant component of chronic neurodegenerative diseases. Cyclooxygenase-2 (COX-2) is expressed in activated microglial cells and appears to be an important source of prostaglandins during inflammatory conditions. To investigate the effect of curcumin on COX-2 gene expression in microglial cells, we treated lipopolysaccharide (LPS)-challenged BV2 microglial cells with various concentrations of curcumin. Curcumin significantly inhibited LPS-mediated induction of COX-2 expression in both mRNA and protein levels in a concentration-dependent manner. COX-2 enzyme activity was also inhibited in accordance with mRNA and protein levels. Furthermore, curcumin markedly inhibited LPS-induced nuclear factor kappaB (NF-kappaB) and activator protein 1 (AP-1) DNA bindings. These data suggest that curcumin suppresses LPS-induced COX-2 gene expression by inhibiting NF-kappaB and AP-1 DNA bindings in BV2 microglial cells.

摘要

炎症是慢性神经退行性疾病的一个重要组成部分。环氧化酶-2(COX-2)在活化的小胶质细胞中表达,并且在炎症状态下似乎是前列腺素的一个重要来源。为了研究姜黄素对小胶质细胞中COX-2基因表达的影响,我们用不同浓度的姜黄素处理脂多糖(LPS)刺激的BV2小胶质细胞。姜黄素以浓度依赖的方式显著抑制LPS介导的COX-2在mRNA和蛋白质水平的表达。COX-2酶活性也与mRNA和蛋白质水平一致地受到抑制。此外,姜黄素显著抑制LPS诱导的核因子κB(NF-κB)和活化蛋白1(AP-1)与DNA的结合。这些数据表明,姜黄素通过抑制BV2小胶质细胞中NF-κB和AP-1与DNA的结合来抑制LPS诱导的COX-2基因表达。

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