ReviewFrontiers in pharmacology2026
Multi-target neuroprotective mechanisms of epigallocatechin-3-gallate (EGCG) in stroke: from molecular pathways to nanomedicine delivery and clinical translation.
Review in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Stroke ranks among the leading global causes of mortality and permanent disability. Its secondary brain injury arises from multiple interrelated pathological cascades, including oxidative stress, neuroinflammation, disrupted autophagy-apoptosis balance, excitotoxicity, iron dyshomeostasis, and blood-brain barrier (BBB) dysfunction. Although intravenous thrombolysis and mechanical thrombectomy have greatly improved the efficacy of acute reperfusion therapy, effective neuroprotective regimens for secondary brain injury remain scarce. Epigallocatechin-3-gallate (EGCG), the most abundant and biologically potent natural catechin extracted from green tea, has attracted extensive research attention in recent years due to its multi-target pharmacological effects. Accumulating evidence demonstrates that EGCG coordinately modulates oxidative stress, neuroinflammation, autophagy-apoptosis homeostasis, excitotoxicity, iron metabolism, and BBB and neurovascular unit (NVU) function to alleviate secondary brain damage and facilitate neurological functional recovery. In addition, EGCG exerts potential adjunct antiplatelet effects
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