2023
DOI: 10.1016/j.heliyon.2023.e13917
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Chlorogenic acid rich in coffee pulp extract suppresses inflammatory status by inhibiting the p38, MAPK, and NF-κB pathways

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Cited by 5 publications
(3 citation statements)
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“…Its activation increases along with the activation of MAPK (Al activates MAPK, as it was already mentioned in this paragraph) and leads to an elevation in the production of pro-inflammatory factors, potentially causing cell damage [ 78 ]. As indicated by the latest research, CGA inhibits NF-κB by suppressing p38 MAPK activation, contributing to the prevention of cell death [ 79 , 80 , 81 ]. It can be concluded that constituents of caffeinated coffee, likely primarily CGA, mitigate the neurotoxicity of Al and thus reduce the risk of neurodegenerative diseases development.…”
Section: Discussionmentioning
confidence: 99%
“…Its activation increases along with the activation of MAPK (Al activates MAPK, as it was already mentioned in this paragraph) and leads to an elevation in the production of pro-inflammatory factors, potentially causing cell damage [ 78 ]. As indicated by the latest research, CGA inhibits NF-κB by suppressing p38 MAPK activation, contributing to the prevention of cell death [ 79 , 80 , 81 ]. It can be concluded that constituents of caffeinated coffee, likely primarily CGA, mitigate the neurotoxicity of Al and thus reduce the risk of neurodegenerative diseases development.…”
Section: Discussionmentioning
confidence: 99%
“…Several mechanisms might explain the beneficial effects of coffee consumption on overall and liver-related mortality. Coffee contains numerous bioactive compounds, including caffeine, chlorogenic acids, and diterpenes, which have been shown to have antiinflammatory, antioxidant, and antifibrotic properties [12][13][14].…”
Section: Discussionmentioning
confidence: 99%
“…Saturated fatty acids, or LPS, induce RAW264.7 cells through the NF-kappa B pathway by binding to toll-like receptor-4 (TRL4). This binding activates the secretion of proinflammatory cytokines (e.g., tumor necrosis factor; TNF-α, interleukin-1beta; IL-1, IL-6) and inflammatory mediators (nitric oxide synthase, iNOS; cyclooxygenase-2, COX-2) [7,8]. A previous study suggested that increasing cytokines and mediators induce decreased insulin signaling [5].…”
Section: Introductionmentioning
confidence: 99%