Dioscin protects against chronic prostatitis through the TLR4/NF-κB pathway.

This study aimed to elucidate the effects and potential mechanisms of dioscin on chronic prostatitis (CP) and . CP models were constructed and and treated with different concentrations of dioscin. Hematoxylin and eosin staining was used to investigate the morphology of the prostate tissues. The concentration of inflammatory factors in prostate tissues was determined by enzyme-linked immunosorbent assay. The release of reactive oxygen species, malondialdehyde, superoxide dismutase, and catalase was measured using detection kits. P69 cell proliferation was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide. Furthermore, the activity of the TLR4/NF-κB signaling pathway was determined by quantitative reverse transcriptase polymerase chain reaction or Western blot assay. Histopathological data suggested that dioscin exerted protective effects against prostate morphological changes. Dioscin inhibits inflammatory cytokines and oxidative stress (OS) in prostate tissues in a concentration-dependent manner. Moreover, dioscin notably inhibited the activation of the TLR4/NF-κB signaling pathway in CP rats. , dioscin remarkably reduced lipopolysaccharide-induced P69 proliferation, inflammation, OS, and TLR4/NF-κB pathway activation in a dose-dependent manner. In conclusion, dioscin exerts a protective effect in CP by decreasing the inflammatory response and OS through the TLR4/NF-κB pathways. Our findings provide a novel latent therapy for dioscin for the treatment and prevention of CP.