2015
DOI: 10.1016/j.intimp.2015.02.015
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Gamma-irradiated resveratrol negatively regulates LPS-induced MAPK and NF-κB signaling through TLR4 in macrophages

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Cited by 51 publications
(44 citation statements)
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“…Thus far, although previous study reported that RSV could reduce neuroinflammation after SAH [22], the molecular mechanisms underlying RSV-dependent anti-inflammatory effects remain obscure. Accumulating studies indicated that RSV could inhibit the activation of TLR4 and the subsequent downstream signaling pathways in different fields [24,25,26]. Thus, we designed this study to confirm the hypothesis that RSV could attenuate SAH-induced EBI by modulating the TLR4 signaling pathway.…”
Section: Introductionmentioning
confidence: 74%
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“…Thus far, although previous study reported that RSV could reduce neuroinflammation after SAH [22], the molecular mechanisms underlying RSV-dependent anti-inflammatory effects remain obscure. Accumulating studies indicated that RSV could inhibit the activation of TLR4 and the subsequent downstream signaling pathways in different fields [24,25,26]. Thus, we designed this study to confirm the hypothesis that RSV could attenuate SAH-induced EBI by modulating the TLR4 signaling pathway.…”
Section: Introductionmentioning
confidence: 74%
“…Most importantly, mountain evidence have demonstrated the critical role of the TLR4 signaling pathways on initiating an inflammatory response after SAH, and that inhibition of the TLR4 signaling pathways could attenuate microglia-induced neuroinflammation [14,15,30]. Regarding the relationship between RSV and TLR4, accumulating studies indicated that RSV could regulate the TLR4 pathway both in vivo and in vitro [24,26,38,39]. For example, Byun et al (2015) reported that RSV could negatively regulate lipopolysaccharides (LPS)-induced NF-κB signaling through TLR4 in macrophages [26].…”
Section: Discussionmentioning
confidence: 99%
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“…Furthermore, mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERK1/2), c-Jun NH 2 -terminal kinases (JNK) and p38, play important roles in regulation of the inflammatory response by mediators. The signaling pathways of MAPKs can lead to the activation of NF-κB and induce expression of pro-inflammatory genes, including IL-1β, IL-6 and iNOS [911]. …”
Section: Introductionmentioning
confidence: 99%