Correlation of pain with substance P and neurokinin-1 receptor in the L5-S2 spinal cord in rats with chronic nonbacterial prostatitis

The incidence of prostate pain is 90%-95% in prostatitis. The symptoms are persistent, which is prone to relapse and difficult to be cured. It seriously affects the survival and quality of life of patients. This study analyzed the correlation between pain and substance P (SP) and neurokinin-1 receptors (NK-1R) in the L5-S2 spinal cord of chronic nonbacterial prostatitis (CNP) rats, which may give a new way to explore the pathogenesis and treatment of pain in prostatitis. We randomly divided the rats into control group, 45 d group, 60 d group, and 90 d group. After making a rat model with autoimmune method, the paw withdrawal threshold (PWT) was measured, the histomorphological changes in the prostate was observed by transmission electron microscopy and light microscopy. The expression of SP and NK-1R was measured by immunohistochemistry, and the concentrations of tumor necrosis factor-& alpha; (TNF-& alpha;), interleukin-10 (IL-10), interleukin-2 (IL-2), and interleukin-10 (IL-10) were measured by enzyme linked immunosorbent assay (ELISA). Compared with the control group, the PWT was decreased by 34.21%, 41.90% and 64.79%, TNF-& alpha; was increased by 74.19%, 89.45% and 132.15%, IL-10 was increased by 148.88%, 181.95% and 250.74%, IL-2 was increased by 75.97%, 82.15% and 128.57% and IL-10 was increased by 31.04%, 63.28% and 212.99% in the 45 d group, 60 d group and 90 d group respectively. Microscope observation showed the structure of prostate tissue in control group was normal. However, the prostate tissue had obvious inflammatory response with the model extension. The expressions of SP and NK-1R in each model group were significantly higher than the control group. There was a significant correlation between pain and SP in L5-S2 spinal cord in CNP rats. These findings are indicative of a correlation between pain and the expression levels of SP and NK-1R in the L5-S2 spinal cord of CNP rats.