The phytotherapeutic agent, eviprostat, suppresses stromal proliferation and inflammation even after establishment of nonbacterial prostatitis in the rat prostate.

OBJECTIVE: To evaluate the effect of phytotherapeutic agent, Eviprostat, administered after the establishment of nonbacterial prostatitis (NBP) on the stroma-to-epithelium ratio (S/E ratio), inflammatory scores, tissue macrophage infiltration, and cytokines and chemokines levels in prostate tissue and urine.

MATERIALS AND METHODS: Ten-month-old male Wistar rats were castrated and exposed to 17-beta-isomer of estradiol for 30 days to induce NBP. Twenty-five NBP rats were divided into 5 groups: (1) NBP (0) rats sacrificed immediately after the establishment of NBP; (2,3) NBP (30)/control (CTL) and NBP (30)/Eviprostat (EVI) rats fed without or with 0.1% Eviprostat under estradiol-free for 30 days, respectively; and (4,5) NBP (60)/CTL and NBP (60)/EVI rats fed without or with 0.1% Eviprostat under estradiol-free for 60 days, respectively. The S/E ratio, inflammatory scores, and the number of macrophage infiltration in the prostate were assessed. Concentrations of cytokines and chemokines in prostatic tissue and urine were measured by enzyme-linked immunosorbent assay.

RESULTS: The S/E ratio was significantly increased with time until 60 days under estradiol-free condition (P <.001). The S/E ratio and the inflammatory scores in NBP (60)/EVI was significantly lower than that of NBP (60)/CTL (P <.001, and P = .022, respectively). The mean tissue concentration of chemokine ligand 2 (CCL2)/monocyte chemoattractant protein-1 (MCP-1) in NBP (60)/CTL was significantly higher than that in NBP (0) (P = .016), whereas, there was no difference between NBP (60)/EVI and NBP (0). Furthermore, urinary CCL2/MCP-1 was significantly decreased in NBP (60)/EVI as compared with NBP (0) (P = .028).

CONCLUSION: Eviprostat suppresses the stromal proliferation and inflammation in the rat prostate after the establishment of NBP at least partly owing to inhibitory effect on CCL2/MCP-1 production in the prostate.