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Carabrol 通过抑制 I-kappaBalpha 的降解来抑制 LPS 诱导的 RAW 264.7 细胞中一氧化氮合酶的表达,从而使 p38 和 JNK 失活。

Carabrol suppresses LPS-induced nitric oxide synthase expression by inactivation of p38 and JNK via inhibition of I-kappaBalpha degradation in RAW 264.7 cells.

机构信息

Department of Life Science, Research Center for Women's Diseases, Sookmyung Women's University, Seoul 140-742, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2010 Jan 15;391(3):1400-4. doi: 10.1016/j.bbrc.2009.12.073. Epub 2009 Dec 22.

Abstract

Carabrol, isolated from Carpesium macrocephalum, showed anti-inflammatory potential in LPS-induced RAW 264.7 murine macrophages. In present study, carabrol demonstrated the inhibitory activity on pro-inflammatory cytokines such as IL-1beta, IL-6 and TNF-alpha. In addition, mRNA and protein levels of iNOS and COX-2 were reduced by carabrol. Molecular analysis revealed that these suppressive effects were correlated with the inactivation of p38 and JNK via inhibition of NF-kappaB activation. Immunoblotting showed that carabrol suppressed LPS-induced degradation of I-kappaBalpha and decreased nuclear translocation of p65. Taken together, these results suggest that carabrol can be a modulator of pro-inflammatory signal transduction pathway in RAW 264.7 cells.

摘要

从苍耳中分离得到的苍术醇在 LPS 诱导的 RAW 264.7 鼠巨噬细胞中显示出抗炎潜力。在本研究中,苍术醇对促炎细胞因子如 IL-1β、IL-6 和 TNF-α表现出抑制活性。此外,苍术醇还降低了 iNOS 和 COX-2 的 mRNA 和蛋白水平。分子分析表明,这些抑制作用与通过抑制 NF-κB 激活来使 p38 和 JNK 失活有关。免疫印迹表明,苍术醇抑制了 LPS 诱导的 I-κBα降解,并减少了 p65 的核转位。综上所述,这些结果表明苍术醇可以作为 RAW 264.7 细胞中促炎信号转导通路的调节剂。

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