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

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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.

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