2015
DOI: 10.1080/09540105.2015.1086315
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Eupatorium makinoisuppresses toll-like receptor signaling pathways

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Cited by 5 publications
(5 citation statements)
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“…To this end, using the model of lipopolysaccharide (LPS)-stimulated murine microglial BV-2 cells, we firstly determined if incubating cells with LZ-8 would lower the production of pro-inflammatory nitric oxide (NO), prostaglandin E 2 (PGE 2 ) and interleukin-6 (IL-6), as well as protein levels of inducible nitric oxide synthase (iNOS) and type-2 cyclooxygenase (COX-2). It is well-known that toll-like receptor-4 (TLR-4)-mediated nuclear factor-kappa B (NF-κB) triggered by LPS are responsible for initiating inflammatory responses by overexpressing numerous pro-inflammatory mediators as above described (Ahn et al, 2016;Kim et al, 2017;Lu, Yeh, & Ohashi, 2008;Taechowisan, Wanbanjob, Tuntiwachwuttikul, & Liu, 2010). Furthermore, the inflammation-related signaling NF-κB cascade was assessed to explore the underlying mechanisms, including gene expression of NF-κB inhibitor (IκBα) and translocation of NF-κB into nucleus.…”
Section: Introductionmentioning
confidence: 99%
“…To this end, using the model of lipopolysaccharide (LPS)-stimulated murine microglial BV-2 cells, we firstly determined if incubating cells with LZ-8 would lower the production of pro-inflammatory nitric oxide (NO), prostaglandin E 2 (PGE 2 ) and interleukin-6 (IL-6), as well as protein levels of inducible nitric oxide synthase (iNOS) and type-2 cyclooxygenase (COX-2). It is well-known that toll-like receptor-4 (TLR-4)-mediated nuclear factor-kappa B (NF-κB) triggered by LPS are responsible for initiating inflammatory responses by overexpressing numerous pro-inflammatory mediators as above described (Ahn et al, 2016;Kim et al, 2017;Lu, Yeh, & Ohashi, 2008;Taechowisan, Wanbanjob, Tuntiwachwuttikul, & Liu, 2010). Furthermore, the inflammation-related signaling NF-κB cascade was assessed to explore the underlying mechanisms, including gene expression of NF-κB inhibitor (IκBα) and translocation of NF-κB into nucleus.…”
Section: Introductionmentioning
confidence: 99%
“…Toxicity of EPA would not be a cause of any observed changes in experiments under a concentration of 50 μM, therefore, all subsequent experiments utilized 30 μM EPA. TLR signaling pathways can trigger the activation of NF-κB, which induces the activation of target genes involved in inflammation (Ahn, Kim, Hong, Gu, Shin, Paek et al 2016;Hacker & Karin, 2006). Therefore, NF-κB activation induced by several TLR agonists was used as the readout for the activation of TLRs.…”
Section: Resultsmentioning
confidence: 99%
“…Epithelial cells are a major interaction site between the host and the environment and they are involved in the regulation of innate mucosal immunity through different pathways, including specific receptors, such as Toll-like receptors (TLRs) (Ahn et al, 2016;Maldonada-Contreras & McCormick, 2011). TLRs have been shown to play an essential role in host immune defense.…”
Section: Discussionmentioning
confidence: 99%