Choi Hye-Jin, Park Jung-Hwan, Lee Bong Ho, Chee Hee Youn, Lee Kyung Bok, Oh Sang-Muk
Department of Biochemistry, College of Medicine, Konyang University, 685 Gasuwon-dong, Seo-gu, Daejeon, 302-832, South Korea.
Appl Biochem Biotechnol. 2014 Jun;173(4):957-67. doi: 10.1007/s12010-014-0910-6. Epub 2014 Apr 18.
Dieckol, extracted from brown algae, Ecklonia cava, is suggested to elicit anti-inflammatory or anti-tumorigenic activities. However, dieckol-mediated regulatory mechanism for inflammatory response still remains elusive. Here, we show that dieckol suppressed lipopolysaccharide (LPS)-induced inducible nitric oxide synthase (iNOS) expression in mouse leukemic macrophage Raw264.7 cells. Also, dieckol decreased LPS-induced both nitric oxide (NO) production and iNOS promoter-driven transcriptional activity in a dose-dependent manner. On the other hand, LPS-mediated NF-κB activity was inhibited by dieckol treatment. Moreover, results revealed that dieckol diminished LPS-mediated p65 nuclear translocation or IκBα phosphorylation dose-dependently, and reduced LPS-induced phosphorylation of mitogen-activated protein kinases (MAPKs), significantly p38MAPK. Collectively, these findings suggest that dieckol acts as a negative regulator of LPS-mediated iNOS induction through suppression of NF-κB activity, implying a mechanistic role of dieckol in regulation of inflammatory response.
从褐藻海蕴中提取的二eckol被认为具有抗炎或抗肿瘤活性。然而,二eckol介导的炎症反应调节机制仍不清楚。在这里,我们表明二eckol抑制脂多糖(LPS)诱导的小鼠白血病巨噬细胞Raw264.7细胞中诱导型一氧化氮合酶(iNOS)的表达。此外,二eckol以剂量依赖性方式降低LPS诱导的一氧化氮(NO)产生和iNOS启动子驱动的转录活性。另一方面,二eckol处理抑制了LPS介导的NF-κB活性。此外,结果显示二eckol剂量依赖性地减少LPS介导的p65核转位或IκBα磷酸化,并显著降低LPS诱导的丝裂原活化蛋白激酶(MAPKs)磷酸化,特别是p38MAPK。总的来说,这些发现表明二eckol通过抑制NF-κB活性作为LPS介导的iNOS诱导的负调节因子,这意味着二eckol在炎症反应调节中具有机制作用。