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首页> 外文期刊>Inflammation research: Official journal of the European Histamine Research Society >The phenyl-thiophenyl propenone RK-I-123 reduces the levels of reactive oxygen species and suppresses the activation of NF-κB and AP-1 and IL-8 expression in Helicobacter pylori-infected gastric epithelial AGS cells
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The phenyl-thiophenyl propenone RK-I-123 reduces the levels of reactive oxygen species and suppresses the activation of NF-κB and AP-1 and IL-8 expression in Helicobacter pylori-infected gastric epithelial AGS cells

机译:苯基-硫代苯基丙烯酮RK-I-123降低了活性氧的水平,并抑制了幽门螺杆菌感染的胃上皮AGS细胞中NF-κB和AP-1和IL-8表达的激活

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摘要

Objective: To investigate whether the phenyl-thiophenyl propenone RK-I-123 suppresses interleukin-8 (IL-8) expression and activation of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-κB [NF-κB] and activator protein-1 [AP-1]) by reducing reactive oxygen species (ROS) levels in Helicobacter pylori-infected gastric epithelial cells. Material: Helicobacter pylori in Korean isolates, human gastric epithelial AGS cells. Treatment: AGS cells pretreated with or without RK-I-123 were cultured in the presence of H. pylori at a bacterium/cell ratio of 300:1. Methods: Reactive oxygen species and IL-8 levels were determined by dichlorofluorescein fluorescence and enzyme-linked immunosorbent assay. The IL-8 mRNA expression was analyzed by the real-time reverse transcription-polymerase chain reaction (RT-PCR). The MAPK and IκBα levels were determined by western blotting. The activation of NF-κB and AP-1 was determined by the electrophoretic mobility shift assay. Results: Helicobacter pylori induced an increase in ROS and IL-8 expression and activation of MAPKs and transcription factors (NF-κB and AP-1) together with the degradation of IκBα in AGS cells, all of which were inhibited by RK-I-123. Conclusions: The RK-I-123 suppressed the H. pylori-induced IL-8 expression and activation of MAPKs, NF-κB, and AP-1 by reducing ROS levels in AGS cells. The RK-I-123 may be a potential candidate for the treatment of H. pylori-induced gastric inflammation.
机译:目的:研究苯基-硫代苯基丙烯酮RK-I-123是否抑制白介素8(IL-8)的表达以及丝裂原活化蛋白激酶(MAPK)和转录因子(核因子-κB[NF-κB]和激活蛋白1 [AP-1])可通过降低幽门螺杆菌感染的胃上皮细胞中的活性氧(ROS)水平来实现。材料:韩国分离株中的幽门螺杆菌,人胃上皮AGS细胞。处理:在幽门螺杆菌的存在下,以300:1的细菌/细胞比例培养经或不经RK-I-123预处理的AGS细胞。方法:用二氯荧光素荧光和酶联免疫吸附法测定活性氧和IL-8水平。通过实时逆转录-聚合酶链反应(RT-PCR)分析IL-8 mRNA的表达。通过蛋白质印迹法测定MAPK和IκBα水平。 NF-κB和AP-1的激活通过电泳迁移率变动分析确定。结果:幽门螺杆菌诱导AGS细胞中ROS和IL-8表达增加,MAPKs和转录因子(NF-κB和AP-1)活化以及IκBα降解,所有这些均被RK-I-抑制123。结论:RK-I-123通过降低AGS细胞中的ROS水平抑制了幽门螺杆菌诱导的IL-8表达以及MAPKs,NF-κB和AP-1的激活。 RK-I-123可能是治疗幽门螺杆菌诱导的胃炎症的潜在候选者。

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