Investigates EGCG's regulatory impact on ovarian function in PCOS mice, revealing new therapeutic potentials.
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder that causes reproductive dysfunction and is often accompanied by insulin resistance and metabolic abnormalities, thereby increasing long-term cardiovascular risk. Current therapeutic strategies mainly focus on symptomatic management and present limitations with prolonged use. Epigallocatechin gallate (EGCG), the main bioactive polyphenol in green tea, has anti-inflammatory, antioxidant, and metabolic regulatory properties. However, its molecular mechanisms in promoting ovarian health and quality in PCOS remain incompletely understood. In this research, we established a PCOS mice model via DHEA induction and subsequently treated the animals with EGCG. Ovarian transcriptomic profiling was performed using RNA sequencing (RNA-seq) to investigate EGCG-mediated gene expression changes. Comparative gene expression analysis revealed 278 genes with differential expression between the EGCG intervention group and the PCOS model group, with 98 genes displaying increased expression and 180 showing decreased expression, indicative of profound transcriptional remodeling induced by EGCG. Functional analysis revealed significant upregulation of several metabolism- and cellular function–related genes, such as Vpreb1b, Pifo, Ldlrad1, Tmem196, and Cyp2b10, while genes including Ces2a, Wnt10b, Sfrp4, S100g, and Odaph were markedly downregulated. Collectively, these findings demonstrate that EGCG exerts broad regulatory effects on ovarian biological processes by modulating key metabolic and functional gene pathways, providing novel molecular insights into the therapeutic potential of EGCG as a targeted intervention for PCOS.
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Xinger Liang (2026) studied this question.
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