title: The role of K ATP channels on ischemia-reperfusion injury in the rat testis.
abstract: OBJECTIVE
  To investigate the participation of K(ATP) channels on the ischemia-reperfusion (IR)-induced apoptosis in the rat testis.
  
  
  METHODS
  Eight-week-old male Sprague-Dawley rats were divided into three groups: control and IR rats without or with cromakalim (300 μg/kg intraperitoneally), 30 min before the induction of ischemia. The right testicular artery and vein were clamped to induce ischemia in the testis. Sixty minutes after the ischemia, a 24h period of reperfusion followed. Then, expressions of K(IR)6.1, K(IR)6.2, caspase-3, PARP, Fas, FasL, and K(IR)6.1 and K(IR)6.2 mRNAs were investigated by Western blot analyses and real-time PCR methods, respectively. Furthermore, testicular tissues were processed for histological evaluation and TUNEL staining.
  
  
  RESULTS
  Expressions of K(IR)6.1 protein and mRNA were more than 10-fold of those of K(IR)6.2 protein and mRNA in the testis. IR significantly increased the expressions of K(IR)6.1 protein and mRNA as well as K(IR)6.2 mRNA, caspase-3, and TUNEL index in the testis compared to the control. PARP expressions were significantly lower in the IR group than those of the control. Histologically, severe acute germ cell damage was observed in the IR testis. Treatment with cromakalim ameliorated these parameters compared to the non-treated IR group. There were no significant differences on Fas, FasL and protein level of K(IR)6.2 expressions between any of the groups.
  
  
  CONCLUSIONS
  Treatment with cromakalim has a protective effect against IR-induced testicular damage via activating K(ATP) channels. This is the first study to give evidence for the advantageous effect of cromakalim in the germ cell-specific apoptosis induced by testicular IR.
authors.affiliation: Division of Urology, Department of Surgery, Tottori University School of Medicine, 36-1 Nishimachi, Yonago, 683-8503, Japan.
authors.forename: Panagiota
authors.initials: P
authors.lastname: Tsounapi
authors.forename: Motoaki
authors.initials: M
authors.lastname: Saito
authors.forename: Fotios
authors.initials: F
authors.lastname: Dimitriadis
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Kitatani
authors.forename: Yukako
authors.initials: Y
authors.lastname: Kinoshita
authors.forename: Kohei
authors.initials: K
authors.lastname: Shomori
authors.forename: Atsushi
authors.initials: A
authors.lastname: Takenaka
authors.forename: Keisuke
authors.initials: K
authors.lastname: Satoh
mesh_terms: D000199:Actins / Q000235:genetics; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D019806:Cromakalim / Q000627:therapeutic use; D004789:Enzyme Activation; D053222:Fas Ligand Protein / Q000235:genetics; D005786:Gene Expression Regulation; D005854:Germ Cells / Q000187:drug effects / Q000473:pathology; D054086:KATP Channels / Q000235:genetics / Q000378:metabolism*; D008297:Male; D011065:Poly(ADP-ribose) Polymerases / Q000235:genetics; D024661:Potassium Channels, Inwardly Rectifying / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D013737:Testis / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D014665:Vasodilator Agents / Q000627:therapeutic use; D000099161:Kcnj11 Channel
chemical_list: D000199:Actins; D053148:Caspase 3; D019806:Cromakalim; D053222:Fas Ligand Protein; D054086:KATP Channels; D011065:Poly(ADP-ribose) Polymerases; D024661:Potassium Channels, Inwardly Rectifying; D012333:RNA, Messenger; D014665:Vasodilator Agents; D000099161:Kcnj11 Channel; C092520:uK-ATP-1 potassium channel