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ارايه پوستر- درمان
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کد مقاله
1450
منابع مقاله
عنوان
EGCG and the Modulation of Angiogenesis in Polycystic Ovary Syndrome: Mechanisms and Therapeutic Implications
نویسندگان
Laleh Talebi - Bahman Rashidi
چکیده
Background: Polycystic ovary syndrome (PCOS) is a common endocrine-metabolic disorder and a major cause of anovulatory infertility, often associated with hyperandrogenism and abnormal ovarian angiogenesis. Dysregulated angiogenesis, driven by increased vascular endothelial growth factor (VEGF), plays an important role in the pathophysiology of PCOS(1, 2). Epigallocatechin-3-gallate (EGCG), the major bioactive catechin in green tea, has been shown to possess antiangiogenic, anti-inflammatory, and antioxidant properties(3). This review evaluates the therapeutic potential and molecular mechanisms of EGCG in modulating abnormal ovarian angiogenesis in PCOS. Method: Comprehensive search of electronic databases (PubMed/MEDLINE, Scopus, Web of Science, and Embase) for relevant peer-reviewed studies was conducted up to 2026. In vitro, in vivo and clinical trials studies related to green tea and benign and malignant female disorders were synthesized and analyzed. Finding: Evidence suggests that EGCG exerts its antiangiogenic effects by reducing the expression and secretion of proangiogenic mediators, particularly VEGF, VEGFR-2, and bFGF, through specific signaling pathways such as PI3K/Akt/mTOR, MAPK/ERK, TGF-β/Smad, and PKA-CREB(4). Systematic evaluations have shown improvements in ovarian histology and hormonal profiles in PCOS animals with green tea extract(5). Conclusion: EGCG can effectively modulate pathological angiogenesis in PCOS by targeting VEGF-mediated signaling pathways. It is a promising natural adjuvant therapeutic agent although further clinical trials are necessary to validate bioavailability, optimal dosage, and human clinical efficacy. Keywords: epigallocatechin gallate, Polycystic Ovary Syndrome, Vascular Endothelial Growth Factors, Angiogenesis, Ovary
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ثمین همایش، سامانه مدیریت همایش ها و جشنواره ها - نگارش 44.12.4