Protective effects of the green tea polyphenol (−)-epigallocatechin gallate against hippocampal neuronal damage after transient global ischemia in gerbils

Lee, Seong‐Ryong; Suh, Seong-Il; Kim, Sang-Pyo

doi:10.1016/s0304-3940(00)01159-9

Cited by 215 publications

(105 citation statements)

References 15 publications

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“…For example, a Ginkgo biloba extract has been shown to protect hippocampal neurons against NO-and b-amyloidinduced neurotoxicity (120) and studies have demonstrated that the consumption of green tea may have a beneficial effect in reducing the risk of Parkinson's disease (121)(122)(123)(124) . In agreement with the latter study, tea extracts and pure (-)-epigallocatechin 3-gallate have been shown to attenuate 6-hydroxydopamine-induced toxicity (125) , to protect against hippocampal injury during transient global ischaemia (126) and to prevent nigral damage induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (127) . The death of nigral neurons in Parkinson's disease is thought to involve the formation of the endogenous neurotoxin 5-S-cysteinyl-dopamine and its oxidation product dihydrobenzothiazine (128,129) (Fig.…”

Section: Inhibition Of Toxin-induced Neuronal Injurysupporting

confidence: 61%

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

Spencer

2010

Proc. Nutr. Soc.

143

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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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Section: Inhibition Of Toxin-induced Neuronal Injurysupporting

confidence: 61%

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

Spencer

2010

Proc. Nutr. Soc.

143

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“…For example, a Ginkgo biloba extract has been shown to protect hippocampal neurons from nitric oxide-and beta-amyloid-induced neurotoxicity [65] and studies have demonstrated that the consumption of green tea may have beneficial effect in reducing the risk of Parkinson's disease [16]. In agreement with the latter study, tea extracts and (-)-epigallocatechin-3-gallate (EGCG) have also been shown to attenuate 6-hydroxydopamineinduced toxicity [61], to protect against hippocampal injury during transient global ischemia [56] and to prevent nigral damage induced by MPTP [60]. The death of nigral neurons in Parkinson's disease is thought to involve the formation of the endogenous neurotoxin, 5-S-cysteinyl-dopamine [108,109].…”

Section: Protection Against Neuronal Injury Induced By Neurotoxinsmentioning

confidence: 75%

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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“…Flavanols (e.g., epicatechin (EC) and catechin) and their monomers/oligomers/polymers, known as procyanidins, compose a major category of secondary polyphenolic plant metabolites. Mounting evidence suggests a protective role for various polyphenols and flavonoids in cerebral ischemia (Lee et al, 2004;Lee et al, 2000;Shah et al, 2005;Shin et al, 2006;Simonyi et al, 2005). It is noteworthy also that flavanols have been shown to improve vasorelaxation (Duarte et al, 1993;Karim et al, 2000).…”

Section: Introductionmentioning

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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Protective effects of the green tea polyphenol (−)-epigallocatechin gallate against hippocampal neuronal damage after transient global ischemia in gerbils

Cited by 215 publications

References 15 publications

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

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

The neuroprotective potential of flavonoids: a multiplicity of effects

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

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