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Inhibition of TNF-induced interleukin-6 gene expression by barley (Hordeum vulgare) ethanol extract in BV-2 microglia

机译:BV-2小胶质细胞中大麦(Hordeum Vulgare)乙醇提取物的TNF诱导的TNF诱导的白细胞介素-6基因表达

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BackgroundInflammation in the central nervous system is closely associated with pathological neurodegenerative diseases as well as psychiatric disorders. Prolonged activation of microglia can produce many inflammatory mediators, which may result in pathological neurotoxic side effects. Interleukin (IL)-6 serves as a hallmark of the injured brain.ObjectiveWhole grains are known to contain many bioactive components. However, little information is available about anti-neuroinflammatory effects of grains in the CNS. This study aims to investigate the effect of Hordeum vulgare ethanol extract (HVE) on the suppression of IL-6 expression in BV2 microglia.MethodsInhibitory effects of HVE on IL-6 expression were analyzed by immunoblot anaysis, immunofluoresce microscopic analysis, reverse transcription-polymerase chain reaction, and luciferase promoter reporter assay.ResultsHVE inhibited TNF-induced phosphorylation of IKK/, IB, and p65/RelA NF-B. TNF-induced IL-6 mRNA expression and promoter activity were reduced by HVE. Point mutation of NF-B-binding site within the IL-6 gene promoter abolished TNF-induced reporter activity, whereas exogenous expression of p65 NF-B enhanced IL-6 promoter activity.ConclusionNF-B-binding site within the IL-6 promoter region is a HVE target element involved in the inhibition of TNF-induced IL-6 gene transcription. HVE inhibits TNF-induced IL-6 expression via suppression of NF-B signaling in BV2 microglial cells.
机译:中枢神经系统中的背景炎症与病理神经退行性疾病以及精神疾病密切相关。延长激活的微胶质细胞可以产生许多炎症介质,这可能导致病理神经毒性副作用。白细胞介素(IL)-6用作受伤脑的标志。已知含有许多生物活性组分的根本血液晶粒。但是,在CNS中谷物的抗神经炎性作用很少有信息。本研究旨在探讨HORDEUM恒星乙醇提取物(HVE)对BV2微胶质细胞IL-6表达的抑制的影响。通过免疫列表AAYSIS,免疫功能微观分析,逆转录 - 聚合酶分析IL-6表达的水平抑制。链反应,荧光素酶启动子报告总分析。抑制IKK /,IB和P65 / Rela NF-B的TNF诱导的TNF磷酸化。通过HVE降低了TNF诱导的IL-6 mRNA表达和启动子活性。 IL-6基因启动子内NF-B结合位点的点突变废除了TNF诱导的报告活性,而P65 NF-B增强IL-6启动子活性的外源表达。IL-6启动子内的ClusionnF-B结合位点区域是涉及抑制TNF诱导的IL-6基因转录的肝脏靶元素。通过在BV2微胶质细胞中抑制NF-B信号传导,HVE抑制TNF诱导的IL-6表达。

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