The alteration of inflammatory markers and apoptosis on chronic prostatitis induced by estrogen and androgen

The age-related decline of the testosterone-to-estrogen (T-to-E-2) ratio in serum is associated with the increased prevalence of prostatic inflammation. The goal of the study was to induce prostatic inflammation with E-2 and androgen treatment and to explore the inflammatory markers and apoptosis on prostatitis. Castrated SD rats were treated with E-2 and different doses of androgens to achieve an elevated concentration of E-2 and a wide range of the androgen-to-E-2 ratio in serum. Inflammatory markers TNF-alpha, COX-2 and MIP-1 alpha were immunohistochemically stained. Apoptosis detection was evaluated by TUNEL staining. E-2, T and DHT concentrations in serum were measured, and the relative weight of the prostate and seminal vesicles were determined. T was anti-inflammatory at the doses which normalized or over stimulated the growth of the prostate and seminal vesicles. Experimentally, prostatitis induced by E-2 alone increased the prostatic levels of the inflammatory markers TNF-a, COX-2 and MIP-1a. As signs of anti-estrogenic actions, androgens dose-dependently decreased the expression of TNF-alpha, COX-2 and MIP-1 alpha. Prostatitis induced by E-2 alone caused extensive apoptosis in the castrate-resistant cells and E-2-induced apoptosis occurred dependently of T manipulation. Estrogen-alone-induced inflammatory response could promote the expression of inflammatory markers; however, T supplementation reduces the expression of inflammatory markers and E-2-induced apoptosis occurs dependently on T manipulation in prostatitis.