title: All-trans-retinoic acid ameliorates the inflammation by inducing transforming growth factor beta 1 and interleukin 10 in mouse epididymitis.
abstract: OBJECTIVE
  Epididymitis, one of the most common urological diseases, can lead to the destruction of the epididymal duct and cause transient or permanent sterility. The aim of this study was to investigate the functions and related mechanisms of all trans retinoic acid (atRA) in alleviating the acute inflammation of epididymitis.
  
  
  METHODS
  The mouse model of the epididymitis was induced by injecting Escherichia coli into the cauda epididymis. atRA was administrated for five consecutive days through intraperitoneal injection. The expression levels of inflammatory cytokines were measured by real-time PCR and Western blot. In addition, cultured primary mouse epididymal epithelial cells were treated with different concentrations of atRA and RAR antagonists to identify whether the effect of atRA was mediated through RAR.
  
  
  RESULTS
  Our results demonstrate that atRA ameliorates the inflammation in mouse epididymitis by decreasing the expression of the pro-inflammatory cytokines and increasing the expression of anti-inflammatory factors including TGF-β1 and IL-10. Our results show that the upregulating effect of atRA on TGF-β1 was mediated by RARα, and the enhancing effect of atRA on IL-10 expression was mediated via RARβ.
  
  
  CONCLUSIONS
  These new results suggest that atRA is involved in regulating the inflammatory response of epididymis.
authors.affiliation: State Key Laboratory of Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Cao
authors.forename: Weigan
authors.initials: W
authors.lastname: Chen
authors.forename: Xiaoxuan
authors.initials: X
authors.lastname: Liang
authors.forename: Jinlian
authors.initials: J
authors.lastname: Zhou
authors.forename: Chao
authors.initials: C
authors.lastname: Wei
authors.forename: Sheng
authors.initials: S
authors.lastname: Cui
authors.forename: Jiali
authors.initials: J
authors.lastname: Liu
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004822:Epididymis / Q000382:microbiology / Q000473:pathology; D004823:Epididymitis / Q000188:drug therapy* / Q000382:microbiology; D004926:Escherichia coli / Q000472:pathogenicity; D004927:Escherichia coli Infections / Q000473:pathology; D007249:Inflammation / Q000188:drug therapy; D016753:Interleukin-10 / Q000096:biosynthesis*; D008297:Male; D051379:Mice; D018168:Receptors, Retinoic Acid / Q000378:metabolism; D000072482:Retinoic Acid Receptor alpha; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis*; D014212:Tretinoin / Q000627:therapeutic use*; D015854:Up-Regulation
chemical_list: D000893:Anti-Inflammatory Agents; C000607072:Rara protein, mouse; D018168:Receptors, Retinoic Acid; D000072482:Retinoic Acid Receptor alpha; D053773:Transforming Growth Factor beta1; C082925:retinoic acid receptor beta; D016753:Interleukin-10; D014212:Tretinoin
keywords: Epididymal epithelium; IL-10; TGF-β1; epididymitis; retinoic acid