ReviewPharmacological reports : PR2025
Green tea's secret weapon: a review on the protective effects of epigallocatechin-3-gallate against ischemia/reperfusion damage.
Review in Pharmacological reports : PR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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.
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.
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0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigallocatechin gallate (EGCG), a major polyphenol in green tea, has gained attention for its therapeutic potential in ischemia/reperfusion (I/R) injury—a condition in which restored blood flow to ischemic tissue paradoxically causes oxidative stress, inflammation, and cell death. EGCG exhibits potent antioxidant, anti-inflammatory, and anti-apoptotic properties that help mitigate these effects through modulation of various molecular signaling pathways. A key mechanism is the activation of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway, which enhances Akt phosphorylation and endothelial nitric oxide synthase (eNOS) activity, thereby promoting vasodilation and improving tissue perfusion. EGCG also influences the Akt/AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR) signaling axis, regulating cellular stress responses and promoting cell survival. It modulates the apoptotic balance by upregulating anti-apoptotic B-cell lymphoma 2 (Bcl-2) and downregulating pro-apoptotic Bax, thereby reducing programmed cell death in I/R-damaged tissues. Additionally, EGCG regulates autophagy, preventing excessive autophagic activity while supporting protective autophagy. It reduces oxidative stress by lowering lipid peroxidation and increasing antioxidant enzymes such as Mn-SOD and catalase. EGCG’s anti-inflammatory effects include decreasing neutrophil infiltration and pro-inflammatory cytokine production during reperfusion. Collectively, these actions make EGCG a promising therapeutic agent for attenuating I/R-induced injury. This review explores the molecular mechanisms behind EGCG’s protective effects and its potential for clinical application in I/R-related diseases.Clinical trial number Not applicable.
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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.