慢性骨盆疼痛综合征模型 z-bo 2020-12-04 366

　　Objective: To construct a C57BL/6 mouse model of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS), and explore its mechanical pain threshold and autophagy-related microtubule light chain protein LC3 and substrate protein p62 The expression level changes with the time of modeling, providing animal experimental evidence for CP/CPPS pain and autophagy level research. Methods: Thirty-six male C57BL/6 mice were randomly divided into blank group, control group and model group. The model group was injected subcutaneously with a suspension of rat prostaglandin extract and complete Freund’s adjuvant at multiple points. CP/CPPS mouse model. The pathological changes of the prostate were observed by HE staining, the mechanical pain threshold of the pelvic area was measured by Von Frey fiber, the expression levels of LC3 and p62 were detected by immunohistochemical staining, and the average optical density was calculated by Image Pro Plus 6.0 software. Results: HE staining showed that the model group mice developed chronic prostatitis, manifested as different degrees of epithelial hyperplasia and lymphocyte invasion, and prostatic intraepithelial neoplasia (PIN) appeared in the prostate at 6 months after the experiment, which appeared as basal Membrane disappearance and nuclear atypia were obvious. The blank group and the control group showed normal histological morphology. Compared with the blank group and the control group, the mechanical pain threshold of the model group gradually decreased with the prolonging of the modeling time [initial pain threshold was (0.35±0.154) g, at week 22 was (0.008±0.000) g], the difference was significant ( P<0.05). The expression levels of LC3 and p62 gradually increased [LC3, p62 average optical density values were respectively, the first month: (2.767±0.464)%, (2.872±1.642)%; the sixth month: (13.501±1.900)%, (9.070±0.490)%], the difference is significant (P<0.05).

　　 Conclusion: The CP/CPPS model was successfully established, and PIN appeared in the 6th month after modeling. The mechanical pain threshold of mice in the model group gradually decreased with the prolongation of the modeling time, and the expression of LC3 and p62 gradually increased, indicating that the CP/CPPS inflammatory microenvironment promoted the generation and aggravation of pain, and increased the level of autophagy in the prostate in mice, and the occurrence and development of PIN closely related.