Investigating the impact of gut microbiota-derived metabolites on benign prostatic hyperplasia using network pharmacology approaches

This study employs a network pharmacology approach to elucidate the intricate "Microbiota-Substrate-Metabolite-Target" (M-S-M-T) network in Benign Prostatic Hyperplasia (BPH), identifying key hub genes (AKT1, IL-6, IL-1B), signaling pathways (PI3K/Akt, AGE-RAGE, HIF-1), and gut microbiota-derived metabolites (butyrate, propionate, TMAO) as central regulators. It further characterizes the functional significance of the Bifidobacterium-tryptophan and Clostridium sporogenes-tyrosine axes, highlighting their probiotic potential for microbiota-targeted BPH therapy. While demonstrating the therapeutic promise of modulating the gut microbiome, the study underscores the need for future experimental validation to decipher the precise mechanistic links within the M-S-M-T network and its role in BPH pathogenesis CONCLUSION: IL-6, AKT1, and IL-1B serve as the primary targets through which gut microbiota metabolites exert their therapeutic effects on benign prostatic hyperplasia.