ArticleNeurochemical research2017
Epigallocatechin Gallate Attenuates β-Amyloid Generation and Oxidative Stress Involvement of PPARγ in N2a/APP695 Cells.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 60 citations in OpenAlex.
- Epigallocatechin-3-Gallate Inhibits Oxidative Stress Through the Keap1/Nrf2 Signaling Pathway to Improve Alzheimer Disease.Molecular neurobiology · 2025Review
- Epigallocatechin-3-gallate therapeutic potential in human diseases: molecular mechanisms and clinical studies.Molecular biomedicine · 2024Review
- The Combined Effect of Green Tea, Saffron, Resveratrol, and Citicoline against Neurodegeneration Induced by Oxidative Stress in anOxidative medicine and cellular longevity · 2024Article
- The relationship between hypoxia and Alzheimer's disease: an updated review.Frontiers in aging neuroscience · 2024Review
- Neuro-Nutraceutical Polyphenols: How Far Are We?Antioxidants (Basel, Switzerland) · 2023Review
- Impact of Nut Consumption on Cognition across the Lifespan.Nutrients · 2023Review
- Diet in the Prevention of Alzheimer's Disease: Current Knowledge and Future Research Requirements.Nutrients · 2022Review
- Article
- Epigallocatechin-3-Gallate (EGCG): New Therapeutic Perspectives for Neuroprotection, Aging, and Neuroinflammation for the Modern Age.Biomolecules · 2022Review
- Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases.Frontiers in pharmacology · 2022Review
- Impact of Phytochemicals on PPAR Receptors: Implications for Disease Treatments.PPAR research · 2022Review
- Rapid Identification of 3,6'-Disinapoyl Sucrose Metabolites in Alzheimer's Disease Model Mice Using UHPLC-Orbitrap Mass Spectrometry.Molecules (Basel, Switzerland) · 2021Article
- Review
- Epigallocatechin-3-gallate improves chronic alcohol-induced cognitive dysfunction in rats by interfering with neuro-inflammatory, cell death and oxido-nitrosative cascade.Metabolic brain disease · 2021Article
- Dual Role of Phenyl Amides from Hempseed on BACE 1, PPARγ, and PGC-1α in N2a-APP Cells.Journal of natural products · 2021Article
- Green Tea Polyphenol Epigallocatechin-Gallate in Amyloid Aggregation and Neurodegenerative Diseases.Frontiers in neuroscience · 2021Review
- Potential Therapeutic Role of Phytochemicals to Mitigate Mitochondrial Dysfunctions in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Ginsenoside Rg1 reduces β‑amyloid levels by inhibiting CDΚ5‑induced PPARγ phosphorylation in a neuron model of Alzheimer's disease.Molecular medicine reports · 2020Article
- Mitochondrial Dysfunction, Oxidative Stress, and Neuroinflammation: Intertwined Roads to Neurodegeneration.Antioxidants (Basel, Switzerland) · 2020Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accumulation of β-amyloid (Aβ) peptide plaques is a major pathogenic event in Alzheimer's disease (AD). Aβ is a cleaved fragment of APP via BACE1, which is the rate-limiting enzyme in APP processing and Aβ generation. Nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) is considered to be a potential target for AD treatment, because of its potent antioxidant and inhibitory effects on Aβ production by negatively regulating BACE1. Epigallocatechin gallate (EGCG), a highly active catechin found in green tea, is known to enhance metabolic activity and cognitive ability in the mice model of AD. To investigate whether the therapeutic effect of EGCG is related to the PPARγ pathway, we analysed the alterations in the intracellular molecular expression of PPARγ after EGCG treatment in the N2a/APP695 cell line. In this study, we observed that EGCG attenuated Aβ generation in N2a/APP695 cells, such as the PPARγ agonist, pioglitazone, by suppressing the transcription and translation of BACE1 and that its effect was attenuated by the PPARγ inhibitor, GW9662. Intriguingly, EGCG significantly reinforced the activity of PPARγ by promoting its mRNA and protein expressions in N2a/APP695 cells. Moreover, EGCG also decreased the expression of pro-apoptotic proteins (Bax, caspase-3), reduced the activity of the anti-inflammatory agent NF-κB and inhibited the oxidative stress by decreasing the levels of ROS and MDA and increasing the expression of MnSOD. Co-administration of GW9662 also significantly decreased the EGCG-mediated neuroprotective effect evidenced by the increase in oxidative stress and inflammatory markers. The therapeutic efficacy of EGCG in AD may be derived from the up-regulation of PPARγ mRNA and protein expressions.
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Registered trials
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