Uptake and metabolism of epicatechin and its access to the brain after oral ingestion

Mohsen, Manal M Abd El; Kuhnle, Gunter; Rechner, A.; Schroeter, Hagen; Rose, Sarah; Jenner, Peter; Rice‐Evans, Catherine

doi:10.1016/s0891-5849(02)01137-1

Cited by 342 publications

(223 citation statements)

References 28 publications

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“…For example, EGCG has been shown to reducing H 2 O 2 and ferrous ion-induced lipid peroxidation in gerbil brain homogenates and to inhibit lipid peroxidation in kidney and liver tissue after induction of oxidative stress with bromotrichloromethane (36, 37). These compounds easily reach brain tissue after oral ingestion to initiate and potentially reduce oxidative stress and inflammation, making them extremely attractive therapeutic compounds, given the lack of a neuronal morphophysiological barrier to GTP access (38,39). The findings presented in this study provide the first indication that oral GTP administration attenuates not only the oxidative and inflammatory mechanisms associated with IH during sleep but also prevents IH-induced spatial learning deficits in the rat.…”

Section: Discussionmentioning

confidence: 67%

Green Tea Catechin Polyphenols Attenuate Behavioral and Oxidative Responses to Intermittent Hypoxia

Burckhardt

Gozal²,

Dayyat³

et al. 2008

Am J Respir Crit Care Med

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Rationale: The intermittent hypoxia (IH) that characterizes sleepdisordered breathing impairs spatial learning and increases NADPH oxidase activity and oxidative stress in rodents. We hypothesized that green tea catechin polyphenols (GTPs) may attenuate IHinduced neurobehavioral deficits by reducing IH-induced NADPH oxidase expression, lipid peroxidation, and inflammation. Objectives: To assess the effects of GTP administered in drinking water on the cognitive, inflammatory, and oxidative responses to long-term (.14 d) IH during sleep in male Sprague-Dawley rats. Methods: Cognitive assessments were conducted in the Morris water maze. We measured levels and expression of malondialdehyde (MDA), prostaglandin E 2 , p47 phox subunit of NADPH oxidase, receptor for advanced glycation end products (RAGE), and glial fibrillary acidic protein expression in rodent brain tissue. Measurements and Main Results: GTP treatment prevented IH-induced decreases in spatial bias for the hidden platform during the Morris water maze probe trails as well as IH-induced increases in p47phox expression within the hippocampal CA1 region. In untreated animals, IH exposure was associated with doubling of cortical MDA levels in comparison to room air control animals, and GTP-treated animals exposed to IH showed a 40% reduction in MDA levels. Increases in brain RAGE and glial fibrillary acidic protein expression were observed in IH-exposed animals, and these increases were attenuated in animals treated with GTP. Conclusions: Oral GTP attenuates IH-induced spatial learning deficits and mitigates IH-induced oxidative stress through multiple beneficial effects on oxidant pathways. Because oxidative processes underlie neurocognitive deficits associated with IH, the potential therapeutic role of GTP in sleep-disordered breathing deserves further exploration.

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Section: Discussionmentioning

confidence: 67%

Green Tea Catechin Polyphenols Attenuate Behavioral and Oxidative Responses to Intermittent Hypoxia

Burckhardt

Gozal²,

Dayyat³

et al. 2008

Am J Respir Crit Care Med

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“…Another criterion of STAIR is that the drug must cross the blood-brain barrier. Available evidence indicates that EC does cross the blood-brain barrier (Abd El Mohsen et al, 2002), as epicatechin glucuronide and 3 0 -O-methyl epicatechin glucuronide have been observed in rat brain for up to 10 days after oral administration of EC (van Praag et al, 2007). Furthermore, after transient ischemia, the blood-brain barrier is likely to be more permeable, especially in the surrounding ischemic region.…”

Section: Discussionmentioning

confidence: 99%

The Flavanol (−)-Epicatechin Prevents Stroke Damage through the Nrf2/HO1 Pathway

Shah

Ahmad

et al. 2010

J Cereb Blood Flow Metab

208

125

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Epidemiologic studies have shown that foods rich in polyphenols, such as flavanols, can lower the risk of ischemic heart disease; however, the mechanism of protection has not been clearly established. In this study, we investigated whether epicatechin (EC), a flavanol in cocoa and tea, is protective against brain ischemic damage in mice. Wild-type mice pretreated orally with 5, 15, or 30 mg/kg EC before middle cerebral artery occlusion (MCAO) had significantly smaller brain infarcts and decreased neurologic deficit scores (NDS) than did the vehicle-treated group. Mice that were posttreated with 30 mg/kg of EC at 3.5 hours after MCAO also had significantly smaller brain infarcts and decreased NDS. Similarly, WT mice pretreated with 30 mg/kg of EC and subjected to N-methyl-D-aspartate (NMDA)-induced excitotoxicity had significantly smaller lesion volumes. Cell viability assays with neuronal cultures further confirmed that EC could protect neurons against oxidative insults. Interestingly, the EC-associated neuroprotection was mostly abolished in mice lacking the enzyme heme oxygenase 1 (HO1) or the transcriptional factor Nrf2, and in neurons derived from these knockout mice. These results suggest that EC exerts part of its beneficial effect through activation of Nrf2 and an increase in the neuroprotective HO1 enzyme.

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“…The tea flavanol EGCG has been reported to access the brain after oral administration to mice [166]. Furthermore, oral ingestion of pure epicatechin resulted in the detection of epicatechin glucuronide and 3 0 -O-methyl-epicatechin glucuronide in rat brain tissue [3]. Anthocyanidins have also been detected in the brain after oral administration [53,168], with several anthocyanidins being identified in different regions of rat brain after the animals were fed with blueberry [12].…”

Section: Flavonoid Metabolism and Access To The Brainmentioning

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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Uptake and metabolism of epicatechin and its access to the brain after oral ingestion

Cited by 342 publications

References 28 publications

Green Tea Catechin Polyphenols Attenuate Behavioral and Oxidative Responses to Intermittent Hypoxia

Green Tea Catechin Polyphenols Attenuate Behavioral and Oxidative Responses to Intermittent Hypoxia

The Flavanol (−)-Epicatechin Prevents Stroke Damage through the Nrf2/HO1 Pathway

The interactions of flavonoids within neuronal signalling pathways

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