Abstract:

Objective The pathogenesis of EAP in rats based on the TLR4/NF-κB?NLRP3 inflammasome signaling pathway was explored. Methods Randomly divide 12 male SD rats into 4 groups using the number table， namely normal group （N）， model group （M）， Caspase-1 inhibitor group （Caspase-1）， and NLRP3 inhibitor MCC950 group （NLRP3）， with 3 rats in each group. After drug intervention， relevant indicators were observed by using HE staining， ELISA， WB methods. Results Compared with the N group， the M group rats had showed significant damage in prostate gland structure and infiltration of inflammatory cells. Compared with group N， the expression of TLR4， P?NF-κB P65， NLRP3， ASC， Cleaced?Caspase-1， Cleaced?IL?1β， and IL?18 proteins in the prostate tissue of group M rats had increased（P < 0.01）. Compared with group M， the expression of TLR4， P?NF-κB P65， NLRP3， ASC， Cleaced?Caspase-1， Cleaced?IL?1β， and IL?18 proteins in the NLRP3 and Caspase?1 groups had significantly reduced（P < 0.01）. The serum levels of IL?1 β， IL?6， IL?8， IL?17A， IL?18， IFN?γ， and TNF?α in group M rats had been significantly higher than those in group N（P < 0.01）. But the serum levels of IL?10 had been slightly lower and no statistical significance. The serum levels of IL?1β， IL?6， IL?8， IL?17A， IL?18， IFN?γ， and TNF?α in group M rats had been lower than those in group N（P < 0.01 or P < 0.05）， the serum IL?10 level had increased（P < 0.01）. Conclusion The activation of TLR4/NF-κB-NLRP3 inflammasome signaling pathway promotes the occurrence and development of prostatitis in EAP rats.

Key words: chronic prostatitis, chronic pelvic pain syndrome, NLRP3 inflammasome, TLR4/NF-κB-NLRP3 inflammasome signaling pathway, inflammatory factor