Rapamycin-induced autophagy attenuates hormone-imbalance-induced chronic non-bacterial prostatitis in rats via the inhibition of NLRP3 inflammasome-mediated inflammation

Chronic non-bacterial prostatitis (CNBP) is a common urinary disease and no standard treatments are available at present. Although autophagy serves an important role in a variety of chronic diseases, its role in CNBP is yet to be fully elucidated. Therefore, the present study aimed to investigate the effects of rapamycin-induced autophagy on CNBP by establishing a rat model. In the present study, a total of 30 male Sprague-Dawley rats were randomly divided into three groups (n=10 per group): i) Control, in which rats underwent a sham operation; ii) the model (CNBP), in which rats were castrated and administered 17-estradiol (0.25 mg/kg via subcutaneous injection) for 30 consecutive days; and iii) rapamycin treatment, in which rats were employed in accordance with the CNBP model, but also received a daily intraperitoneal injection of rapamycin (1 mg/kg) from the 16th day post-surgery for 15 days. Alterations in histology and the levels of autophagy-associated markers, and components of the NLRP3 inflammasome, were measured in the prostate tissues of the rats. The levels of molecules located further downstream of the NLRP3 inflammasome pathway, including interleukin (IL)-1 and IL-18, were also measured. The results demonstrated that, compared with the control group, increased infiltration levels of inflammatory cells and glandular epithelial degeneration were observed in the prostate tissues of rats with CNBP. Furthermore, a significant increase in the concentration of IL-1 and IL-18 in the serum, as well as the increased expression levels of NLRP3, ASC and caspase-1 in prostate tissues were also observed. In addition, reductions in the number of autophagosomes and the expression levels of autophagy-associated, including microtubule-associated protein 1 light chain 3 (LC3B) and Beclin 1, were also detected in the CNBP group; however, treatment with rapamycin reversed these effects. Collectively, the findings of the present study indicated that the NLRP3 inflammasome-mediated inflammatory response was activated by a hormonal imbalance in the prostate glands of rats; however, these effects may be suppressed via rapamycin-induced autophagy.