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<p>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.</p><p><b>Clinical trial number</b> Not applicable.</p>

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Green tea’s secret weapon: a review on the protective effects of epigallocatechin-3-gallate against ischemia/reperfusion damage

  • 期刊论文

  • 发表日期：

    2025年9月5日

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  • Yingxin Wang,
  • Ying Cao,
  • Yue Zhao

摘要

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.