Naringin mitigates experimental autoimmune prostatitis by modulating oxidative stress and the NLRP3 inflammasome via the PPAR-γ/NF-κB pathway.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is a debilitating condition characterized by pelvic pain and discomfort, necessitating the exploration of effective therapeutic strategies. This study aimed to elucidate the therapeutic potential of naringin (NAR) in addressing CP/CPPS by examining its role in modulating oxidative stress (OS) and the NLRP3 inflammasome via the PPARγ/NF-κB signaling pathway. Using both animal and cellular models of CP/CPPS, naringin was administered to mice with experimental autoimmune prostatitis (EAP), and the anti-inflammatory effect of naringin was assessed. Furthermore, cellular assays were performed to investigate the mechanistic pathway underlying the effects of naringin, with a focus on its role in mitigating oxidative stress and suppressing NLRP3 inflammasome activation. The results indicated that naringin significantly reduced inflammation in both models by effectively inhibiting NLRP3 inflammasome activation and restoring cellular homeostasis via oxidative stress modulation linked to the activation of the PPARγ/NF-κB axis. In conclusion, naringin showed promising therapeutic effects in mitigating inflammation associated with CP/CPPS, highlighting its potential as a novel treatment option. Further investigations into the clinical applicability of naringin are needed to fully understand its therapeutic potential in patients suffering from CP/CPPS.