【Animal Modeling】-How to establish a model of chronic pelvic pain syndrome?

  Objective: To establish a C57BL/6 mouse model of chronic pelvic pain syndrome (chronic prostatitis/chronic pelvic pain syndrome, CP/CPPS) and its mechanical pain threshold and autophagy-related microtubule light chain protein LC3 and its substrate Protein p62, grade. The model time provides an experimental basis for animal studies on CP/CPPS pain and autophagy levels.

  Method: 36 male C57BL/6 mice were randomly divided into blank group, control group and model group. The mice in the model group were injected with a suspension of rat prostaglandin extract subcutaneously, and complete Freund's adjuvant was injected at multiple locations. CP/CPPS mouse model. HE staining was used to observe the pathological changes of the prostate, VonFrey filaments were used to measure the mechanical pain threshold in the pelvic area, and the expression levels of LC3 and p62 were detected by immunohistochemical staining. The average optical density was ImageProPlus 6.0.

  Results: HE staining showed that the mice in the model group developed chronic prostatitis, manifested by epithelial hyperplasia and lymphocyte infiltration, and high-grade prostate intraepithelial neoplasia (PIN) appeared in the prostate 6 months after the experiment. Membrane disappearance and nuclear atypia were obvious. The blank and control group showed normal tissue morphology. Compared with the blank group and the control group, the mechanical pain threshold of the model group gradually decreased with the extension of the modeling time [the initial pain threshold was (0.35±0.154)g, and at week 22 it was (0.008±0.000)g . Meet g], the difference is statistically significant (P\u003c0.05). The expression levels of LC3 and p62 gradually increased [the average optical density values of LC3 and p62 were (2.767±0.464)% and (2.872±1.642)%; the sixth month: (13.501±), respectively. 1.900)%, (9.070±0.490)%], the difference is significant (P\u003c0.05).

  Conclusion: The CP/CPPS model has been successfully established, and the PIN was displayed 6 months after the model was built. The mechanical pain threshold of mice in the model group gradually decreased with the increase of modeling time, and the expression of LC3 and p62 gradually increased. The CP/CPPS inflammatory microenvironment promoted the onset and aggravation of pain, and reduced the degree of pain. improve. The development of autophagy in the mouse prostate is closely related to the development of PIN.