Protective effect of phlorotannins from Eisenia bicyclis against lipopolysaccharide-stimulated inflammation in HepG2 cells
Protective effect of phlorotannins from Eisenia bicyclis against lipopolysaccharide-stimulated inflammation in HepG2 cells
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DOI：
10.1016/j.etap.2013.01.009
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发表时间：
2013-05-01
影响因子：
4.3
通讯作者：
Kim, Young-Mog
中科院分区：
文献类型：
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作者：
Kang, Young-Mi;Eom, Sung-Hwan;Kim, Young-Mog
从双环草中分离得到4个具有生物活性的间苯三酚衍生物，包括间苯三酚（1）、艾可酚（2）、二氧乙烯脱氢艾可酚（3）和狄可酚（4），并通过核磁共振（NMR）对其结构进行了表征。此外，这些化合物的抗炎活性进行了研究对人肝癌细胞系HepG 2细胞由脂多糖（LPS）刺激。研究表明，LPS可诱导HepG 2细胞产生促炎细胞因子如白细胞介素-1 β（IL-1 β）、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α），以及表达炎性介质如环氧合酶-2（考克斯-2）和诱导型一氧化氮合酶（iNOS）。在分离的化合物中，化合物（1）对HepG 2细胞中LPS刺激的炎症反应表现出显著的抑制作用，而没有任何细胞毒性。本文中，化合物（1）抑制促炎细胞因子如IL-1 β、IL-6和TNF-α的产生以及考克斯-2和iNOS的表达。因此，这些结果表明，从E.双环，特别是化合物（1），可用作预防和治疗炎症反应的有益来源。(c)2013爱思唯尔有限公司版权所有。
In this study, four bioactive phloroglucinol derivates including phloroglucinol (1), eckol (2), dioxinodehydroeckol (3), and dieckol (4) were isolated from Eisenia bicyclis and characterized by nuclear magnetic resonance (NMR) spectroscopic methods. Moreover, the anti-inflammatory activity of these compounds was investigated on human hepatoma cell line HepG2 cells stimulated by lipopolysaccharide (LPS). It was demonstrated that LPS can induce the production of pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) as well as the expression of inflammatory mediators as cyclooxygenase-2 (COX-2), and inducible nitric oxide synthases (iNOS) from HepG2 cells. Among isolated compounds, compound (1) exhibited significant inhibition on LPS-stimulated inflammatory responses in HepG2 cells without any cytotoxicity. Herein, compound (1) suppresses the production of pro-inflammatory cytokines such as IL-1 beta, IL-6, and TNF-alpha and the expression of COX-2 and iNOS. Thus, these results indicated that phlorotannins isolated from E. bicyclis, especially compound (1), can be used as a beneficial source for preventing and treating inflammation response. (c) 2013 Elsevier B.V. All rights reserved.