目的：探讨慢性非细菌性前列腺炎（chronic nonbacterial prostatitis，CNP）疼痛的可能机制。方法自身免疫法建立CNP大鼠模型；Von Frey丝检测机械刺激缩足阈（paw withdrawal threshold，PWT）；进行前列腺病理学检查和免疫组化检测前列腺与脊髓L5-S2节段c-fos、TRPV1的表达变化和相关性。结果造模后大鼠PWT下降，与对照组相比差异有统计学意义（P＜0.05）。前列腺呈现炎症反应，在病变范围、淋巴细胞浸润方面都较对照组显著，差异有统计学意义（P＜0.05）。与对照组相比，模型组前列腺与脊髓背角L5-S2中c-fos、TRPV1阳性表达均上调，差异有统计学意义（P＜0.05）。前列腺中与脊髓中的c-fos表达无相关关系（r =0.027，P =0.454）；并且两者的TRPV1表达也无相关关系（r =0.000，P=0.5）。结论 c-fos、TRPV1可能通过脊髓L5-S2节段的表达上调参与了CNP大鼠疼痛的形成和维持。“,”Objective To explore the possible mechanisms of chronic nonbacterial prostatitis pain. Methods The CNP rat model was established by the immune method. The pain threshold were detected by Von Frey filament. The expressions of c-fos and TRPV1 in the prostate and spinal L5- S2 segmental were detected by immunohistochemistry. Results The PWT of rat model group was significantly decreased as compared with that of the control group (P<0.05). There were significant inflammation in prostate tissues of rats. The differences in the scope of lesions and interstitial lymphocytic infiltrates were statistically significant between model group and the control group (P<0.05). The expressions of c-fos and TRPV1 in prostate and spinal cord dorsal horn L5 - S2 in model group were all upregulated remarkably compared with that of the control group (P<0.05). The expression of c-fos and TRPV1 in the prostate had no correlation with that in spinal cord (r =0.027,P =0.454; r = 0.000, P = 0.000). Conclusion Formation of the pain in rats may be associated with upregulation of c-fos and TRPV1 in the spinal L5 - S2 section.