title: The alteration of inflammatory markers and apoptosis on chronic prostatitis induced by estrogen and androgen.
abstract: OBJECTIVE
  The age-related decline of the testosterone-to-estrogen (T-to-E2) ratio in serum is associated with the increased prevalence of prostatic inflammation. The goal of the study was to induce prostatic inflammation with E2 and androgen treatment and to explore the inflammatory markers and apoptosis on prostatitis.
  
  
  METHODS
  Castrated SD rats were treated with E2 and different doses of androgens to achieve an elevated concentration of E2 and a wide range of the androgen-to-E2 ratio in serum. Inflammatory markers TNF-α, COX-2 and MIP-1α were immunohistochemically stained. Apoptosis detection was evaluated by TUNEL staining. E2, T and DHT concentrations in serum were measured, and the relative weight of the prostate and seminal vesicles were determined.
  
  
  RESULTS
  T was anti-inflammatory at the doses which normalized or over stimulated the growth of the prostate and seminal vesicles. Experimentally, prostatitis induced by E2 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-α, COX-2 and MIP-1α. Prostatitis induced by E2 alone caused extensive apoptosis in the castrate-resistant cells and E2-induced apoptosis occurred dependently of T manipulation.
  
  
  CONCLUSIONS
  Estrogen-alone-induced inflammatory response could promote the expression of inflammatory markers; however, T supplementation reduces the expression of inflammatory markers and E2-induced apoptosis occurs dependently on T manipulation in prostatitis.
authors.affiliation: School of Pharmacy, Fudan University, Shanghai, 201203, China.
authors.forename: Yu-ling
authors.initials: YL
authors.lastname: Jia
authors.forename: Xu
authors.initials: X
authors.lastname: Liu
authors.forename: Jian-yan
authors.initials: JY
authors.lastname: Yan
authors.forename: Li-ming
authors.initials: LM
authors.lastname: Chong
authors.forename: Lei
authors.initials: L
authors.lastname: Li
authors.forename: Ai-cui
authors.initials: AC
authors.lastname: Ma
authors.forename: Li
authors.initials: L
authors.lastname: Zhou
authors.forename: Zu-yue
authors.initials: ZY
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis; D001835:Body Weight; D002369:Castration; D054405:Chemokine CCL3 / Q000032:analysis; D002908:Chronic Disease; D051546:Cyclooxygenase 2 / Q000032:analysis; D013196:Dihydrotestosterone / Q000097:blood; D004195:Disease Models, Animal; D004967:Estrogens / Q000009:adverse effects* / Q000097:blood; D008297:Male; D011467:Prostate / Q000737:chemistry*; D011472:Prostatitis / Q000097:blood* / Q000139:chemically induced* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013739:Testosterone / Q000009:adverse effects* / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D054405:Chemokine CCL3; D004967:Estrogens; D014409:Tumor Necrosis Factor-alpha; D013196:Dihydrotestosterone; D013739:Testosterone; D051546:Cyclooxygenase 2