ArticleInternational journal of molecular sciences2011
Modulation of Ca²⁺ signals by epigallocatechin-3-gallate(EGCG) in cultured rat hippocampal neurons.
Article in International journal of molecular sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- A Pilot Study: Comparative Effects of Green Tea Extract and Duloxetine on Oxaliplatin-Induced Allodynia in a Murine Model.Metabolites · 2025Article
- Clinical insights into catechin-based nanomedicine: a review of therapeutic potential in neurodegenerative diseases.3 Biotech · 2025Review
- Role of Cytoskeletal Elements in Regulation of Synaptic Functions: Implications Toward Alzheimer's Disease and Phytochemicals-Based Interventions.Molecular neurobiology · 2024Review
- Neurodegenerative diseases and catechins: (-)-epigallocatechin-3-gallate is a modulator of chronic neuroinflammation and oxidative stress.Frontiers in nutrition · 2024Review
- A Comprehensive Review on Beneficial Effects of Catechins on Secondary Mitochondrial Diseases.International journal of molecular sciences · 2022Review
- Green Tea Catechins, (-)-Catechin Gallate, and (-)-Gallocatechin Gallate are Potent Inhibitors of ABA-Induced Stomatal Closure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Green Tea Suppresses Brain Aging.Molecules (Basel, Switzerland) · 2021Review
- Article
- Green Tea Catechins Trigger Immediate-Early Genes in the Hippocampus and Prevent Cognitive Decline and Lifespan Shortening.Molecules (Basel, Switzerland) · 2020Article
- New Perspectives in Iron Chelation Therapy for the Treatment of Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2018Review
- The role of calcineurin signaling in microcystin-LR triggered neuronal toxicity.Scientific reports · 2015Article
- Polyphenols: multipotent therapeutic agents in neurodegenerative diseases.Oxidative medicine and cellular longevity · 2013Review
- STAT1-deficient mice are resistant to cecal ligation and puncture-induced septic shock.Shock (Augusta, Ga.) · 2012Article
- Inhibition of the intracellular Ca(2+) transporter SERCA (Sarco-Endoplasmic Reticulum Ca(2+)-ATPase) by the natural polyphenol epigallocatechin-3-gallate.Journal of bioenergetics and biomembranes · 2012Article
- Pleiotropic protective effects of phytochemicals in Alzheimer's disease.Oxidative medicine and cellular longevity · 2012Review
- Detailed analysis of apoptosis and delayed luminescence of human leukemia Jurkat T cells after proton irradiation and treatments with oxidant agents and flavonoids.Oxidative medicine and cellular longevity · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Green tea has been receiving considerable attention as a possible neuroprotective agent against neurodegenerative disease. Epigallocatechin-3-gallate (EGCG) is the major compound of green tea. Calcium signaling has profound effects on almost all aspects of neuronal function. Using digital calcium imaging and patch-clamp technique, we determined the effects of EGCG on Ca(2+) signals in hippocampal neurons. The results indicated that EGCG caused a dose-dependent increase in intracellular Ca(2+) ([Ca(2+)](i)). This [Ca(2+)](i) increase was blocked by depleting intracellular Ca(2+) stores with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin and cyclopiazonic acid. Furthermore, EGCG-stimulated increase in [Ca(2+)](i) was abolished following treatment with a PLC inhibitor. However, EGCG inhibited high-voltage activated Ca(2+) currents (I(HVA)) and NMDA-induced inward currents (I(NMDA)). These data suggest that EGCG triggers a cascade of events: it activates phospholipase C (PLC), mobilizes intracellular Ca(2+) stores, raises the cytosolic Ca(2+) levels, and inhibits the VGCC and NMDA receptors-mediated Ca(2+) influx through a process that remains to be determined.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.