EGCG Attenuates AMPA-Induced Intracellular Calcium Increase in Hippocampal Neurons

Bae, Jae Hoon; Mun, Kyo‐Cheol; Park, Won Kyun; Lee, Seung-Ryong; Suh, Seong-Il; Baek, Won-Ki; Yim, Man-Bin; Kwon, Taeg Kyu; Song, Dae‐Kyu

doi:10.1006/bbrc.2002.6372

Cited by 54 publications

(10 citation statements)

References 28 publications

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“… 66 It can also act as an antagonist of glutamine AMPA receptor-mediated responses. 67 These findings suggest that some of the neuroprotective effects of EGCG may occur via an inhibitory effect on glutamate-mediated excitation on neurons by increasing GABA-mediated inhibition. In fact, a number of flavonoids that are structurally related to EGCG (eg, apigenin, quercetin) may act as ligands of the benzodiazepine GABA A receptor site.…”

Section: Resultsmentioning

confidence: 96%

Does Green Tea Induce Hormesis?

et al. 2020

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Green tea, and its principal constituent (–)-epigallocatechin-3-gallate (EGCG), are commonly shown to induce biphasic concentration/dose responses in a broad range of cell types, including non-tumor cells, and tumor cell lines. The most active area of research dealt with an assessment of neural cells with application to neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease cell models, often using preconditioning experimental protocols. The general findings demonstrate EGCG-induced hormetic effects resulting in an enhanced acquired resilience within an adaptive and temporally dependent homeodynamic framework. The biphasic dose responses displayed the typical quantitative features of the hormetic dose response with respect to the amplitude and width of the stimulatory response. These findings provide further evidence for the general occurrence of hormetic dose responses with such responses being independent of the biological model, end point, inducing agent, and mechanism. The biphasic nature of these responses has important implications since it suggests optimal dose ranges for end points of public health and therapeutic applications. These findings indicate the need to assess the entire dose-response continuum in order to better define the nature of the dose response, especially in the low-dose zone where such exposures are common in human populations.

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Section: Resultsmentioning

confidence: 96%

Does Green Tea Induce Hormesis?

et al. 2020

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“…TPs are natural antioxidants extracted from tea with radical eliminating capacity. In addition, EGCG has been reported to scavenge free radicals by directly or indirectly blocking free radical chain reactions, activating intracellular antioxidant enzyme activity [ 29 ], chelating metal ions [ 30 ], reducing lipid peroxidation [ 31 ], and releasing intracellular calcium [ 32 ]. Additionally, EGCG protects neuronal cells against oxidative stress-induced death and apoptosis [ 30 ].…”

Section: Neuroprotective Effects and Mechanisms Of Tea Polyphenolsmentioning

confidence: 99%

Neuroprotective Effects and Mechanisms of Tea Bioactive Components in Neurodegenerative Diseases

Chen

Ze-shi

et al. 2018

Molecules

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As the population ages, neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD) impose a heavy burden on society and families. The pathogeneses of PD and AD are complex. There are no radical cures for the diseases, and existing therapeutic agents for PD and AD have diverse side effects. Tea contains many bioactive components such as polyphenols, theanine, caffeine, and theaflavins. Some investigations of epidemiology have demonstrated that drinking tea can decrease the risk of PD and AD. Tea polyphenols can lower the morbidity of PD and AD by reducing oxidative stress and regulating signaling pathways and metal chelation. Theanine can inhibit the glutamate receptors and regulate the extracellular concentration of glutamine, presenting neuroprotective effects. Additionally, the neuroprotective mechanisms of caffeine and theaflavins may contribute to the ability to antagonize the adenosine receptor A2AR and the antioxidant properties, respectively. Thus, tea bioactive components might be useful for neuronal degeneration treatment in the future. In the present paper, the neuro protection and the mechanisms of tea and its bioactive components are reviewed. Moreover, the potential challenges and future work are also discussed.

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“…Flavonoids have been known to inhibit various ion channels, including Ca 2+ -permeable ion channels [ 7 8 9 ]. Cyanidin-3-glucoside (C3G), a component of anthocyanin, belongs to the flavonoid family.…”

Section: Introductionmentioning

confidence: 99%

Cyanidin-3-glucoside inhibits amyloid β_25–35-induced neuronal cell death in cultured rat hippocampal neurons

Yang

Jeon

Yoon

et al. 2018

Korean J Physiol Pharmacol

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Increasing evidence implicates changes in [Ca2+]i and oxidative stress as causative factors in amyloid beta (Aβ)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting Ca2+ and Zn2+ signaling. The present study aimed to determine whether C3G exerts a protective effect against Aβ25–35-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for Ca2+, Zn2+, MMP and ROS. Treatment with Aβ25–35 (20 µM) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited Aβ25–35-induced [Zn2+]i increases as well as [Ca2+]i increases in the cultured rat hippocampal neurons. C3G also significantly inhibited Aβ25–35-induced mitochondrial depolarization. C3G also blocked the Aβ25–35-induced formation of ROS. In addition, C3G significantly inhibited the Aβ25–35-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid β-induced neuronal cell death by reducing multiple apoptotic signals.

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EGCG Attenuates AMPA-Induced Intracellular Calcium Increase in Hippocampal Neurons

Cited by 54 publications

References 28 publications

Does Green Tea Induce Hormesis?

Does Green Tea Induce Hormesis?

Neuroprotective Effects and Mechanisms of Tea Bioactive Components in Neurodegenerative Diseases

Cyanidin-3-glucoside inhibits amyloid β_25–35-induced neuronal cell death in cultured rat hippocampal neurons

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EGCG Attenuates AMPA-Induced Intracellular Calcium Increase in Hippocampal Neurons

Cited by 54 publications

References 28 publications

Does Green Tea Induce Hormesis?

Does Green Tea Induce Hormesis?

Neuroprotective Effects and Mechanisms of Tea Bioactive Components in Neurodegenerative Diseases

Cyanidin-3-glucoside inhibits amyloid β25–35-induced neuronal cell death in cultured rat hippocampal neurons

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Product

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Cyanidin-3-glucoside inhibits amyloid β_25–35-induced neuronal cell death in cultured rat hippocampal neurons