title: [Androgen may improve erectile function in castrated rats by regulating the ERK1/2 pathway].
abstract: OBJECTIVE
  To investigate the role of the extracellular signal-regulated protein kinase 1/2 (ERK1/2) pathway in erectile dysfunction (ED) caused by the absence of testosterone (T).
  
  
  METHODS
  We randomly divided 30 eight-week-old healthy male SD rats into groups A (control) , B (castration), and C (castration + androgen replacement). The rats in groups B and C were castrated surgically, and those in C injected with T undecanoate (100 mg/kg) at 1 week after castration, while the others with 0.9% normal saline instead. At 1 month after treatment, we determined the serum T level, intracavernous pressure (ICP), and mean carotid arterial pressure (MAP) of the rats, and detected the expressions of ERK1/2 and endothelial nitric oxide synthase (eNOS) by Western blot.
  
  
  RESULTS
  The serum T level was significantly lower in group B ([1.27 ± 0.48] nmol/L) than in A ([17.14 ± 1.07] nmol/L) and C ([16.24 ± 1.90] nmol/L) (P < 0.05), and so were ICP and MAP (P < 0.05). The expression of ERK1/2 showed no statistically significant differences among the three groups (P > 0.05), that of phosphatase ERK1/2 was markedly higher while that of eNOS remarkably lower in group B than in A and C (both P < 0.05).
  
  
  CONCLUSIONS
  Androgen replacement may improve the erectile function of castrated rats by regulating the ERK1/2 pathway.
authors.forename: Kai
authors.initials: K
authors.lastname: Cui
authors.forename: Rui
authors.initials: R
authors.lastname: Li
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Tao
authors.initials: T
authors.lastname: Wang
authors.forename: Shao-gang
authors.initials: SG
authors.lastname: Wang
authors.forename: Zhang-qun
authors.initials: ZQ
authors.lastname: Ye
authors.forename: Ke
authors.initials: K
authors.lastname: Rao
authors.forename: Ji-hong
authors.initials: JH
authors.lastname: Liu
mesh_terms: D000728:Androgens / Q000627:therapeutic use*; D000818:Animals; D015153:Blotting, Western; D007172:Erectile Dysfunction / Q000188:drug therapy / Q000378:metabolism*; D020249:Hormone Replacement Therapy; D020935:MAP Kinase Signaling System; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D009919:Orchiectomy; D010410:Penile Erection; D010413:Penis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013739:Testosterone / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000728:Androgens; D013739:Testosterone; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; C010792:testosterone undecanoate