1. Academic Validation
  2. Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1

Epigallocatechin-3-Gallate Attenuates Benign Prostatic Hyperplasia Development via Regulating Firmicutes to Inhibit Gastric Secretion of Insulin-Like Growth Factor-1

  • Cell Biol Int. 2025 Aug;49(8):952-964. doi: 10.1002/cbin.70032.
Tianye Yang 1 YiQun Shao 2 Zhong Wang 2 Chong Liu 3 Meng Gu 3
Affiliations

Affiliations

  • 1 Department of Emergency, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
  • 2 Department of Urology and Andrology, Gongli Hospital of Shanghai Pudong New Area, Shanghai, China.
  • 3 Department of Urology, Shanghai Ninth People's Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China.
Abstract

Benign prostatic hyperplasia (BPH), a prevalent age-related condition in men, is increasingly linked to metabolic syndrome (MetS) and gut microbiota dysbiosis. This study reveals how Firmicutes-dominant microbial imbalance drives BPH progression via IGF-1 signaling and identifies the green tea polyphenol epigallocatechin-3-gallate (EGCG) as a dual-action therapeutic. Using MetS-BPH mouse models and human prostate cell lines, we demonstrated that BPH-associated gut microbiota-particularly elevated Firmicutes and an increased Firmicutes/Bacteroidetes ratio-promotes prostate hyperplasia by upregulating IGF-1. Both BPH mice and recipient mice transplanted with BPH microbiota showed elevated serum and prostate IGF-1 levels, mirroring findings in human BPH patients. Mechanistically, IGF-1 stimulated prostate cell proliferation (RWPE-1/WPMY-1) and suppressed Apoptosis via PI3K/Akt/mTOR activation, while the IGF-1 antagonist Linsitinib reversed these effects. EGCG emerged as a potent modulator of this gut-prostate axis: it selectively reduced Firmicutes overgrowth in BPH mice, normalized IGF-1 levels, and inhibited downstream PI3K/Akt/mTOR signaling. In fecal microbiota transplantation experiments, EGCG counteracted IGF-1-driven prostate enlargement and microbial dysbiosis, underscoring its dual role in rebalancing gut flora and blocking growth factor pathways. Our findings position EGCG as a promising intervention for MetS-associated BPH, simultaneously targeting microbial dysbiosis and IGF-1 signaling. This study not only elucidates the Firmicutes-IGF-1 axis in BPH pathogenesis but also highlights the therapeutic potential of dietary Polyphenols in metabolic urological disorders.

Keywords

EGCG; Firmicutes; IGF‐1; benign prostatic hyperplasia.

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