The Therapeutic Potential of EGCG and Pro-EGCG in Mitigating Ovarian Hyperstimulation Syndrome: Unraveling the Modulatory Mechanism through the VEGF Pathway

This paper studied the therapeutic effects and mechanisms of (-)-epigallocatechin-3-gallate (EGCG) and its more stable derivative Pro-EGCG in ovarian hyperstimulation syndrome (OHSS), using primary human granulosa-lutein (hGL) cells, the KGN granulosa-like cell line, and a rat OHSS model induced with pregnant mare serum gonadotropin. Across in vitro and in vivo assays, EGCG and Pro-EGCG reduced OHSS progression indicators, including ovarian weight changes, histological findings, and decreased VEGF expression at transcriptomic and proteomic levels, with RNA sequencing supporting VEGF downregulation. Mechanistically, the study reports that EGCG suppresses TGF-β–induced VEGF production by inhibiting the TGF-β/Smad and PKA-CREB signaling pathways, also involving 67-kDa laminin receptor-mediated regulation of PKA-CREB. The paper notes key caveats including use of cell lines and an animal model as proxies and that mechanistic work is based on pathway modulation assays rather than direct clinical efficacy in IVF patients with OHSS. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match mentioning EGCG in female reproductive diseases including endometriosis.

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