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首页> 外文期刊>Inflammation >Thymol inhibits LPS-stimulated inflammatory response via down-regulation of NF-κB and MAPK signaling pathways in mouse mammary epithelial cells.
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Thymol inhibits LPS-stimulated inflammatory response via down-regulation of NF-κB and MAPK signaling pathways in mouse mammary epithelial cells.

机译:麝香草酚通过下调小鼠乳腺上皮细胞中NF-κB和MAPK信号通路来抑制LPS刺激的炎症反应。

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摘要

Thymol is a natural monoterpene phenol primarily found in thyme, oregano, and tangerine peel. It has been shown to possess anti-inflammatory property both in vivo and in vitro. In the present paper, we studied the anti-inflammatory effect of thymol in lipopolysaccharide (LPS)-stimulated mouse mammary epithelial cells (mMECs). The mMECs were stimulated with LPS in the presence or absence of thymol (10, 20, 40 μg/mL). The concentrations of tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-1β in the supernatants of culture were determined using enzyme-linked immunosorbent assay. Cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), extracellular signal-regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), nuclear factor-κB (NF-κB), and inhibitor protein of NF-κB (IκBα) were measured using western blot. The results showed that thymol markedly inhibited the production of TNF-α and IL-6 in LPS-stimulated mMECs. The expression of iNOS and COX-2 was also suppressed by thymol in a dose-dependent manner. Furthermore, thymol blocked the phosphorylation of IκBα, NF-κB p65, ERK, JNK, and p38 mitogen-activated protein kinases (MAPKs) in LPS-stimulated mMECs. These results indicate that thymol exerted anti-inflammatory property in LPS-stimulated mMECs by interfering the activation of NF-κB and MAPK signaling pathways. Thereby, thymol may be a potential therapeutic agent against mastitis.
机译:百里香酚是一种天然的单萜酚,主要存在于百里香,牛至和橘皮中。已显示其在体内和体外均具有抗炎特性。在本文中,我们研究了百里酚在脂多糖(LPS)刺激的小鼠乳腺上皮细胞(mMECs)中的抗炎作用。在有或没有百里酚(10、20、40μg/ mL)的情况下,用LPS刺激mMEC。使用酶联免疫吸附测定法测定培养上清液中肿瘤坏死因子α(TNF-α),白介素(IL)-6和IL-1β的浓度。环氧合酶2(COX-2),诱导型一氧化氮合酶(iNOS),细胞外信号调节蛋白激酶(ERK),c-Jun N端激酶(JNK),核因子-κB(NF-κB)和抑制剂使用蛋白质印迹法检测NF-κB(IκBα)蛋白。结果表明,百里香酚显着抑制LPS刺激的mMECs中TNF-α和IL-6的产生。百里香酚也以剂量依赖性的方式抑制了iNOS和COX-2的表达。此外,百里香酚阻断了LPS刺激的mMEC中IκBα,NF-κBp65,ERK,JNK和p38丝裂原活化蛋白激酶(MAPK)的磷酸化。这些结果表明,百里香酚通过干扰NF-κB和MAPK信号通路的激活,在LPS刺激的mMEC中发挥抗炎作用。因此,百里酚可能是对抗乳腺炎的潜在治疗剂。

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