Effect of the phytotherapeutic agent Eviprostat on 17beta-estradiol-induced nonbacterial inflammation in the rat prostate.

Background: Anti-inflammatory medications have been used for the treatment of chronic prostatitis. The phytotherapeutic agent Eviprostat, a popular treatment for benign prostatic hyperplasia in Japan and Germany, has antioxidant and anti-inflammatory activity. We investigated the effects of the phytotherapeutic agent Eviprostat on prostate inflammation induced in castrated rats by the injection of 17beta-estradiol.

Methods: Ten-month-old male Wistar rats were divided into five groups. Nonbacterial prostatitis was experimentally induced in groups 2-5 by castration followed by daily subcutaneous injection of 17beta-estradiol for 30 days. The rats were orally administered 0.1% Tween-80 (group 2), low-dose Eviprostat (group 3), high-dose Eviprostat (group 4), or cernitin pollen extract (group 5) for the last 2 weeks of 17beta-estradiol administration. Sham-operated rats (group 1) were orally administered 0.1% Tween-80. On the 31st day after surgery, the weight of the prostate and the levels of prostatic proinflammatory cytokines as well as the oxidative-stress marker malondialdehyde were determined and histological alterations noted.

Results: Experimentally induced nonbacterial prostatitis led to a significant decrease in prostate weight and increases in malondialdehyde and proinflammatory cytokine levels. Eviprostat significantly suppressed the increases in malondialdehyde and cytokine levels without affecting prostate weight. Histologically, nonbacterial prostatitis was evident in the lateral lobe of the prostate, and Eviprostat treatment significantly suppressed the severity of the lesion.

Conclusions: Eviprostat, which has effective antioxidant and anti-inflammatory activities in the prostate, may be useful for the clinical treatment of chronic prostatitis. These activities of Eviprostat may also contribute to the amelioration of prostate inflammation in BPH patients. Prostate 69: 1404-1410, 2009. (c) 2009 Wiley-Liss, Inc.