The green tea polyphenol (−)-epigallocatechin gallate attenuates β-amyloid-induced neurotoxicity in cultured hippocampal neurons

Choi, Young-Taeg; Jung, Chul-Ho; Lee, Seong‐Ryong; Bae, Jae‐Hoon; Baek, Won-Ki; Suh, Min-Ho; Park, Jonghan; Park, Chanwoo; Suh, Seong-Il

doi:10.1016/s0024-3205(01)01438-2

Cited by 309 publications

(194 citation statements)

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“…Further support comes from in vitro studies, where green tea and black tea extracts were shown to exhibit potent neuroprotection against 6-OHDA-induced damage in NB SH-SY5Y and PC12 cells, via inhibition of nuclear translocation of the OS and inflammatory-responsive transcription factor NF-B (10). Moreover, EGCG or Ginkgo biloba extract, known to be enriched with flavonoids, protects hippocampal neurons from ␤-amyloid-derived peptide (A␤)-or nitric oxide-induced neurotoxicity (18,19,39). Furthermore, the polyphenol epicatechin was shown to attenuate neurotoxicity induced by oxidized low density lipoprotein in mouse-derived striatal neurons (30).…”

Section: Discussionmentioning

confidence: 99%

“…17). These findings are supported by in vitro studies, where EGCG or the Ginkgo biloba extract were shown to prevent amyloid ␤ peptide (A␤)-induced neurotoxicity in cultured hippocampal neurons (18,19) and in PC12 cells 2 Moreover, the flavonoid epicatechin was shown to attenuate neurotoxicity induced by oxidized low density lipoprotein in mouse-derived striatal neurons (20).…”

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confidence: 85%

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Involvement of Protein Kinase C Activation and Cell Survival/ Cell Cycle Genes in Green Tea Polyphenol (−)-Epigallocatechin 3-Gallate Neuroprotective Action

Levites¹,

Amit²,

Youdim³

et al. 2002

Journal of Biological Chemistry

387

324

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Studies from our laboratory have demonstrated that the major green tea polyphenol, (؊)-epigallocatechin 3-gallate (EGCG), exerts potent neuroprotective actions in the mice model of Parkinson's disease. These studies were extended to neuronal cell culture employing the parkinsonism-inducing neurotoxin, 6-hydroxydopamine (6-OHDA). Pretreatment with EGCG (0.1-10 M) attenuated human neuroblastoma (NB) SH-SY5Y cell death, induced by a 24-h exposure to 6-OHDA (50 M). Potential cell signaling candidates involved in this neuroprotective effect were further examined. EGCG restored the reduced protein kinase C (PKC) and extracellular signal-regulated kinases (ERK1/2) activities caused by 6-OHDA toxicity. However, the neuroprotective effect of EGCG on cell survival was abolished by pretreatment with PKC inhibitor GF 109203X (1 M). Because EGCG increased phosphorylated PKC, we suggest that PKC isoenzymes are involved in the neuroprotective action of EGCG against 6-OHDA. In addition, gene expression analysis revealed that EGCG prevented both the 6-OHDA-induced expression of several mRNAs, such as Bax, Bad, and Mdm2, and the decrease in Bcl-2, Bcl-w, and Bcl-x L . These results suggest that the neuroprotective mechanism of EGCG against oxidative stressinduced cell death includes stimulation of PKC and modulation of cell survival/cell cycle genes.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 85%

Involvement of Protein Kinase C Activation and Cell Survival/ Cell Cycle Genes in Green Tea Polyphenol (−)-Epigallocatechin 3-Gallate Neuroprotective Action

Levites¹,

Amit²,

Youdim³

et al. 2002

Journal of Biological Chemistry

387

324

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“…EGCG reduced the toxicity of Aβ in pheochromocytoma and neuroblastoma cell models [66,67]. Green tea extract decreased the formation of amyloid deposits [68,69] and the loss of spatial learning ability in a mouse model of [70].…”

Section: New Strategies For Intervention In Amyloidogenesis: Egcgmentioning

confidence: 95%

Natural Compounds May Open New Routes to Treatment of Amyloid Diseases

Bieschke

2013

Neurotherapeutics

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Protein misfolding disorders, such as Alzheimer's disease and Parkinson's disease, have in common that a protein accumulates in an insoluble form in the affected tissue. The process of aggregation follows a mechanism of seeded polymerization. Although the toxic species is still not well defined, the process, rather than the end product, of fibril formation is likely the main culprit in amyloid toxicity. These findings suggest that therapeutic strategies directed against the protein misfolding cascade should focus on depleting aggregation intermediates rather than on large fibrillar aggregates. Recent studies involving natural compounds have suggested new intervention strategies. The polyphenol epi-gallocatechine-3-gallate (EGCG), the main polyphenol in Camilla sinensis, binds directly to a large number of proteins that are involved in protein misfolding diseases and inhibits their fibrillization. Instead, it promotes the formation of stable, spherical aggregates. These spherical aggregates are not cytotoxic, have a lower β-sheet content than fibrils, and do not catalyze fibril formation. Correspondingly, epi-gallocatechine-3-gallate remodels amyloid fibrils into aggregates with the same properties. Derivatives of Orcein, which is a phenoxazine dye that can be isolated from the lichen Roccella tinctoria, form a second promising class of natural compounds. They accelerate fibril formation of the Alzheimer's disease-related amyloid-beta peptide. At the same time these compounds deplete oligomeric and protofibrillar forms of the peptide. These compounds may serve as proof-of-principle for the strategies of promoting and redirecting fibril formation. Both may emerge as two promising new therapeutic approaches to intervening into protein misfolding processes.

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“…EGCG is the prominent and most active component of green tea catechins [74,75]. It acts as an antioxidant [76] and attenuates lipid peroxidation caused by various forms of free radicals in biological systems [77]. Tea leaves have also been reported for their cognition-enhancing ability [78] and for abating oxidative changes associated with aging [79].…”

Section: Green Teamentioning

confidence: 99%

Traditional Korean East Asian Medicines and Herbal Formulations for Cognitive Impairment

Kumar

Song

et al. 2013

Molecules

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Abstract:Hanbang, the Traditional Korean Medicine (TKM), is an inseparable component of Korean culture both within the country, and further afield. Korean traditional herbs have been used medicinally to treat sickness and injury for thousands of years. Oriental medicine reflects our ancestor's wisdom and experience, and as the elderly population in Korea is rapidly increasing, so is the importance of their health problems. The proportion of the population who are over 65 years of age is expected to increase to 24.3% by 2031. Cognitive impairment is common with increasing age, and efforts are made to retain and restore the cognition ability of the elderly. Herbal materials have been considered for this purpose because of their low adverse effects and their cognitive-enhancing or anti-dementia activities. Herbal materials are reported to contain several active compounds that have effects on cognitive function. Here, we enumerate evidence linking TKMs which have shown benefits in memory improvements. Moreover, we have also listed Korean herbal formulations which have been the subject of scientific reports relating to memory improvement.

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The green tea polyphenol (−)-epigallocatechin gallate attenuates β-amyloid-induced neurotoxicity in cultured hippocampal neurons

Cited by 309 publications

References 0 publications

Involvement of Protein Kinase C Activation and Cell Survival/ Cell Cycle Genes in Green Tea Polyphenol (−)-Epigallocatechin 3-Gallate Neuroprotective Action

Involvement of Protein Kinase C Activation and Cell Survival/ Cell Cycle Genes in Green Tea Polyphenol (−)-Epigallocatechin 3-Gallate Neuroprotective Action

Natural Compounds May Open New Routes to Treatment of Amyloid Diseases

Traditional Korean East Asian Medicines and Herbal Formulations for Cognitive Impairment

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