title: Inhibition of interleukin-6 attenuates erectile dysfunction in a rat model of nerve-sparing radical prostatectomy.
abstract: BACKGROUND
  The precise mechanisms underlying erectile dysfunction (ED) occurring after cavernous nerve (CN)-sparing surgery remain to be determined. Aim.  To evaluate the expression of interleukin-6 (IL-6) and IL-6 receptor (IL-6R) after CN injury, and the effect of inhibiting IL-6 bioactivity on nerve injury-related ED.
  
  
  METHODS
  Male Sprague-Dawley rats were divided into three groups: sham operation; bilateral CN dissection without crushing or cutting; and bilateral CN resection. In the interventional experiment, male rats underwent bilateral CN dissection, and anti-rat IL-6 antibody in phosphate-buffered saline (PBS) or vehicle alone was injected intraperitoneally immediately and 24 hours after CN dissection.
  
  
  METHODS
  One, 3, 7, 28, and 56 days after surgery, the expression of IL-6 and IL-6R in the major pelvic ganglion (MPG) was examined by real-time polymerase chain reaction. In the interventional experiment, erectile function was assessed by determining intracavernous pressure divided by arterial pressure (ICP/AP) during electrical pelvic nerve stimulation at 4 weeks after surgery in the anti-IL-6-injected rats and PBS-injected rats. The degree of nerve injury was also evaluated by retrograde dye tracing with Fluorogold.
  
  
  RESULTS
  The expression levels of IL-6 and IL-6R were increased in the early period of CN injury, as compared with the sham group. IL-6 expression on day 1 was particularly enhanced. Four weeks after CN dissection, the anti-IL-6 group had greater ICP/AP and more FG-positive cells than the PBS group.
  
  
  CONCLUSIONS
  Expression levels of IL-6 in the MPG were increased in the acute phase following CN injury. Inhibition of IL-6 bioactivity attenuated ED following CN dissection. Thus, the suppression of excess inflammatory responses in the acute phase may lead to improvements in ED occurring after nerve-sparing radical prostatectomy.
authors.affiliation: Department of Urology, Sapporo Medical University School of Medicine, Sapporo, Japan Department of Urology, Tohoku University Graduate School of Medicine, Sendai, Japan. yamashita@uro.med.tohoku.ac.jp
authors.forename: Shinichi
authors.initials: S
authors.lastname: Yamashita
authors.forename: Ryuichi
authors.initials: R
authors.lastname: Kato
authors.forename: Ko
authors.initials: K
authors.lastname: Kobayashi
authors.forename: Shin-Ichi
authors.initials: S
authors.lastname: Hisasue
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Arai
authors.forename: Taiji
authors.initials: T
authors.lastname: Tsukamoto
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D007172:Erectile Dysfunction / Q000209:etiology / Q000276:immunology*; D015850:Interleukin-6 / Q000096:biosynthesis*; D008297:Male; D010410:Penile Erection / Q000276:immunology*; D011468:Prostatectomy / Q000009:adverse effects* / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D019947:Receptors, Interleukin-6 / Q000096:biosynthesis*; D000093242:Interleukin-6 Inhibitors
chemical_list: D015850:Interleukin-6; D019947:Receptors, Interleukin-6; D000093242:Interleukin-6 Inhibitors