Britanin suppresses LPS-induced nitric oxide, PGE2 and cytokine production via NF-κB and MAPK inactivation in RAW 264.7 cells

Britanin suppresses LPS-induced nitric oxide, PGE2 and cytokine production via NF-κB and MAPK inactivation in RAW 264.7 cells
复制标题

DOI:
10.1016/j.intimp.2012.12.005
复制
发表时间:
2013-02-01
影响因子:
5.6
通讯作者:
Lee, Eunkyung
Lee, Eunkyung
中科院分区:
医学2区
文献类型:
--
作者:
Park, Hyo-Hyun;Kim, Mi Jin;Lee, Eunkyung

文献摘要

被引文献

相似文献

从旋覆花中分离得到的旋覆花素的生物学特性尚不清楚。本研究在前期研究旋覆花具有抗炎、平喘作用的基础上,探讨了旋覆花中的活性成分,并在此基础上,采用RAW 264.7细胞模型,研究了旋覆花素对炎症介质、核因子(NF)-κ B和丝裂原活化蛋白(MAP)激酶活性的影响。Britanin可抑制脂多糖(LPS)刺激的RAW264.7细胞产生一氧化氮(NO)和前列腺素E2(PGE(2))沿着,并抑制诱导型一氧化氮合酶(iNOS)和环氧合酶(考克斯)-2的表达。此外,britanin减少促炎细胞因子的释放,如TNF-α,IL-1 β和IL-6。此外,在LPS刺激的RAW 264.7细胞中,MAP激酶(p38和JNK)的磷酸化被britanin抑制。此外,britanin抑制由LPS诱导的NF-κ B B活化,这与Met降解的废除和随后的核p65水平的降低有关。这项研究表明,britanin的抗炎活性可能是由于抑制iNOS和考克斯-2和细胞因子的表达,至少部分,通过减弱磷酸化的MAP激酶和NF-κ B激活通过I κ B α降解在巨噬细胞。我们的结论是,britanin可能通过下调MAP激酶和NF-κ B B介导的巨噬细胞活化来治疗炎症性疾病。(C)2012爱思唯尔有限公司版权所有。
Little is known about the biological properties of britanin, which is isolated from the flowers of Inula japonica (Inulae Flos). Based on our previous studies that Inulae Flos had anti-inflammation and anti-asthmatic activities, we tried to find the bioactive compounds from it. In this study, the anti-inflammatory effects of britanin on the inflammatory mediators as well as on nuclear factor (NF)-kappa B and mitogen-activated protein (MAP) kinase activation were evaluated in RAW 264.7 cells. Britanin inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE(2)) along with the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. In addition, britanin reduced the release of pro-inflammatory cytokines, such as TNF-alpha, IL-1 beta, and IL-6. Furthermore, the phosphorylations of MAP kinases (p38 and JNK) in LPS-stimulated RAW 264.7 cells were suppressed by britanin. Moreover, britanin inhibited the NF-kappa B activation induced by LPS, which was associated with the abrogation of Met degradation and subsequent decreases in nuclear p65 levels. This study suggests that the anti-inflammatory activities of britanin might be attributed to the inhibition of iNOS and COX-2 and cytokine expression at least in part, through the attenuation of the phosphorylations of MAP kinases and NF-kappa B activation via I kappa B alpha degradation in macrophages. We conclude that britanin may have potential for the treatment of inflammatory diseases through the down-regulation of MAP kinases and NF-kappa B mediated activation of macrophages. (C) 2012 Elsevier B.V. All rights reserved.