(−)‐Epigallocatechin gallate inhibits lipopolysaccharide‐induced microglial activation and protects against inflammation‐mediated dopaminergic neuronal injury

Li, Rui; Huang, Yuan; Du, Fang; Le, Weidong

doi:10.1002/jnr.20315

Cited by 192 publications

(111 citation statements)

References 45 publications

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“…Flavonoid-rich blueberry extracts have been observed to inhibit NO, IL-1b and TNF-a production in activated microglia cells [53,54], whilst the flavonol quercetin [17], the flavones wogonin and bacalein [55], the flavanols catechin and epigallocatechin gallate (EGCG) [62], and the isoflavone genistein [125] have all been shown to attenuate microglia and/or astrocyte mediated neuroinflammation via mechanisms that include inhibition of: (1) iNOS and cyclooxygenase (COX-2) expression, (2) NO production, (3) cytokine release, and (4) NADPH oxidase activation and subsequent reactive oxygen species generation, in astrocytes and microglia. Flavonoids may exert these effects via direct modulation of protein and lipid kinase signalling pathways [98,105,130], for example via the inhibition of MAPK signalling cascades, such as p38 or ERK1/2 which regulate both iNOS and TNF-a expression in activated glial cells [9].…”

Section: Inhibition Of Neuroinflammationmentioning

confidence: 99%

The neuroprotective potential of flavonoids: a multiplicity of effects

et al. 2008

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Flavonoids exert a multiplicity of neuroprotective actions within the brain, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation, and the potential to promote memory, learning and cognitive function. These effects appear to be underpinned by two common processes. Firstly, they interact with critical protein and lipid kinase signalling cascades in the brain leading to an inhibition of apoptosis triggered by neurotoxic species and to a promotion of neuronal survival and synaptic plasticity. Secondly, they induce beneficial effects on the vascular system leading to changes in cerebrovascular blood flow capable of causing angiogenesis, neurogenesis and changes in neuronal morphology. Through these mechanisms, the consumption of flavonoid-rich foods throughout life holds the potential to limit neurodegeneration and to prevent or reverse age-dependent loses in cognitive performance. The intense interest in the development of drugs capable of enhancing brain function means that flavonoids may represent important precursor molecules in the quest to develop of a new generation of brain enhancing drugs.

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Section: Inhibition Of Neuroinflammationmentioning

confidence: 99%

The neuroprotective potential of flavonoids: a multiplicity of effects

et al. 2008

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“…The structurallyrelated flavanone hesperetin and other flavonoids appear to be incapable of inhibiting pathways leading to NO production, although they have been found to partially alleviate neuroinflammation through the inhibition of TNFa production (103) . Flavonoids present in blueberry have also been shown to inhibit NO, IL-1b and TNFa production in activated microglia cells (104) , whilst the flavonol quercetin (105) , the flavones wogonin and bacalein (106) , the flavanols catechin and epigallocatechin gallate (107) and the isoflavone genistein (108) have all been shown to attenuate microglia-and/or astrocyte-mediated neuroinflammation via mechanisms that include inhibition of, in astrocytes and microglia: (1) iNOS and cyclooxygenase 2 expression; (2) NO production; (3) cytokine release; (4) NADPH oxidase activation and subsequent reactive oxygen species generation. All these effects appear to depend on an ability to directly modulate protein kinase and lipid kinase signalling pathways (45,46) .…”

Section: Inhibition Of Neuroinflammationmentioning

confidence: 99%

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

Spencer

2010

Proc. Nutr. Soc.

142

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The consumption of flavonoid-rich foods and beverages has been suggested to limit the neurodegeneration associated with a variety of neurological disorders and to prevent or reverse normal or abnormal deteriorations in cognitive performance. Flavonoids mediate these effects via a number of routes, including a potential to protect neurons against injury induced by neurotoxins, an ability to suppress neuroinflammation and a potential to promote memory, learning and cognitive function. Originally, it was thought that such actions were mediated by the antioxidant capacity of flavonoids. However, their limited absorption and their low bioavailability in the brain suggest that this explanation is unlikely. Instead, this multiplicity of effects appears to be underpinned by three separate processes: first, through their interactions with important neuronal and glial signalling cascades in the brain, most notably the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways that regulate prosurvival transcription factors and gene expression; second, through an ability to improve peripheral and cerebral blood flow and to trigger angiogenesis and neurogenesis in the hippocampus; third, by their capacity to directly react with and scavenge neurotoxic species and pro-inflammatory agents produced in the brain as a result of both normal and abnormal brain ageing. The present review explores the potential inhibitory or stimulatory actions of flavonoids within these three systems and describes how such interactions are likely to underlie neurological effects.

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“…Thus far, studies have indicated that flavanols [72,105], flavones [34,87,99,151,186], and flavonols [35] are all capable of inhibiting the release of NO…”

Section: Extracellular Signal-regulated Protein Kinase Pathwaymentioning

confidence: 99%

The interactions of flavonoids within neuronal signalling pathways

2007

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Emerging evidence suggests that dietary phytochemicals, in particular flavonoids, may exert beneficial effects in the central nervous system by protecting neurons against stress-induced injury, by suppressing neuroinflammation and by promoting neurocognitive performance, through changes in synaptic plasticity. It is likely that flavonoids exert such effects in neurons, through selective actions on different components within a number of protein kinase and lipid kinase signalling cascades, such as phosphatidylinositol-3 kinase (PI3K)/Akt, protein kinase C and mitogen-activated protein kinase. This review details the potential inhibitory or stimulatory actions of flavonoids within these pathways, and describes how such interactions are likely to affect cellular function through changes in the activation state of target molecules and/or by modulating gene expression. Although, precise sites of action are presently unknown, their abilities to: (1) bind to ATP binding sites on enzymes and receptors; (2) modulate the activity of kinases directly; (3) affect the function of important phosphatases; (4) preserve neuronal Ca 2+ homeostasis; and (5) modulate signalling cascades lying downstream of kinases, are explored. Future research directions are outlined in relation to their precise site(s) of action within the signalling pathways and the sequence of events that allow them to regulate neuronal function in the central nervous system.

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(−)‐Epigallocatechin gallate inhibits lipopolysaccharide‐induced microglial activation and protects against inflammation‐mediated dopaminergic neuronal injury

Cited by 192 publications

References 45 publications

The neuroprotective potential of flavonoids: a multiplicity of effects

The neuroprotective potential of flavonoids: a multiplicity of effects

Beyond antioxidants: the cellular and molecular interactions of flavonoids and how these underpin their actions on the brain

The interactions of flavonoids within neuronal signalling pathways

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