Tadalafil (TAD) is primarily a treatment drug for erectile dysfunction. Studies have shown that TAD has a therapeutic effect on prostatitis, but the specific mechanism has not been reported. LPS induced RWPE-1 cells to form a model of chronic nonbacterial prostatitis (CNP). Cell activity was measured by MTT assay. Apoptosis was detected by TUNEL assay. Western blot was used to detect the expression of apoptosis-related proteins Bcl-2, Bax, Caspase-3, and cleaved caspase3. ELISA was used to detect the expression of inflammatory cytokines TNF-α, IL-6, and IL-8. GSH, catalase (CAT), and malondialdehyde (MDA) kits were used to detect the expression of oxidative stress-related indicators GSH, CAT, and MDA. Western blot was used to detect the expression of proteins related to Akt/Nrf2 signaling pathway. After different concentrations of TAD were given, the survival rate of LPS-induced RWPE-1 cells decreased, apoptosis increased, and inflammation and oxidative stress decreased. This process is accompanied by the activation of the Akt/Nrf2 signaling pathway. The addition of AKT inhibitor (HY-10249A) reversed the inhibitory effect of TAD on LPS-induced inflammatory response and oxidative stress of RWPE-1 cell. TAD alleviated LPS-induced inflammation and oxidative stress of RWPE-1 cell by regulating the Akt/Nrf2 signaling pathway.
Keywords: Akt/Nrf2 signaling pathway; chronic nonbacterial prostatitis; inflammation; oxidative stress; tadalafil.