An ethyl acetate fraction derived from Houttuynia cordata extract inhibits the production of inflammatory markers by suppressing NF-кB and MAPK activation in lipopolysaccharide-stimulated RAW 264.7 macrophages.
An ethyl acetate fraction derived from Houttuynia cordata extract inhibits the production of inflammatory markers by suppressing NF-кB and MAPK activation in lipopolysaccharide-stimulated RAW 264.7 macrophages.
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DOI：
10.1186/1472-6882-14-234
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发表时间：
2014-07-10
影响因子：
--
通讯作者：
Kim HK
中科院分区：
文献类型：
--
作者：
Chun JM;Nho KJ;Kim HS;Lee AY;Moon BC;Kim HK
鱼腥草Houttuynia cordata Thunb.(三白草科)在传统医学中被用于治疗炎症性疾病。本研究评价了鱼腥草乙酸乙酯提取物(Hce-EA)对内毒素刺激的RAW 264.7巨噬细胞产生炎症介质及激活核因子-κB(NF-κB)和丝裂原活化蛋白激酶(MAPK)的作用。为了检测羟基喜树碱对RAW 264.7细胞促炎细胞因子和炎症介质表达的影响，我们采用了细胞存活率测定、Griess试剂分析、酶联免疫吸附试验、实时定量聚合酶链式反应和免疫印迹分析等方法。HCE-EA可下调细胞内一氧化氮(NO)、前列腺素E_2(PGE_2)、肿瘤坏死因子-α(TN-α)和白介素6(IL-6)的产生，以及诱导型一氧化氮合酶(INOS)和环氧合酶-2(COX-2)的表达。此外，HCE-EA还抑制了NF-κB p65亚基的核转位，这与抑制IκBα(核因子轻多肽基因增强子在B细胞中的抑制物，α)的磷酸化有关。HCE-EA还可减弱MAPKs(p38和JNK)的激活。我们的结果提示，HCE-EA的抗炎作用可能源于通过抑制NF-κB和MAPK信号通路而抑制促炎介质。
Houttuynia cordata Thunb. (Saururaceae) has been used in traditional medicine for treatment of inflammatory diseases. This study evaluated the anti-inflammatory effects of an ethyl acetate fraction derived from a Houttuynia cordata extract (HCE-EA) on the production of inflammatory mediators and the activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. To measure the effects of HCE-EA on pro-inflammatory cytokine and inflammatory mediator’s expression in RAW 264.7 cells, we used the following methods: cell viability assay, Griess reagent assay, enzyme-linked immunosorbent assay, real-time polymerase chain reaction and western blotting analysis. HCE-EA downregulated nitric oxide (NO), prostaglandin E2 (PGE2), tumor necrosis factor-α (TNF-α), and interleukin (IL-6) production in the cells, as well as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression. Furthermore, HCE-EA suppressed nuclear translocation of the NF-κB p65 subunit, which correlated with an inhibitory effect on IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha) phosphorylation. HCE-EA also attenuated the activation of MAPKs (p38 and JNK). Our results suggest that the anti-inflammatory properties of HCE-EA may stem from the inhibition of pro-inflammatory mediators via suppression of NF-κB and MAPK signaling pathways.
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影响因子：
5.6
作者：
Park, Hyo-Hyun;Kim, Mi Jin;Lee, Eunkyung
通讯作者：
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DOI：
10.1016/j.bbapap.2005.08.017
发表时间：
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影响因子：
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作者：
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影响因子：
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影响因子：
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作者：
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