The role of K ATP channels on ischemia-reperfusion injury in the rat testis

Panagiota Tsounapi, Motoaki Saito, Fotios Dimitriadis, Kazuyuki Kitatani, Yukako Kinoshita, Kohei Shomori, Atsushi Takenaka, Keisuke Satoh

研究成果: Article査読

15 被引用数 (Scopus)


Aims: To investigate the participation of K ATP channels on the ischemia-reperfusion (IR)-induced apoptosis in the rat testis. Main 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 24 h period of reperfusion followed. Then, expressions of K IR6.1, K IR6.2, caspase-3, PARP, Fas, FasL, and K IR6.1 and K IR6.2 mRNAs were investigated by Western blot analyses and real-time PCR methods, respectively. Furthermore, testicular tissues were processed for histological evaluation and TUNEL staining. Key findings: Expressions of K IR6.1 protein and mRNA were more than 10-fold of those of K IR6.2 protein and mRNA in the testis. IR significantly increased the expressions of K IR6.1 protein and mRNA as well as K IR6.2 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 IR6.2 expressions between any of the groups. Significance: 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.

ジャーナルLife Sciences
出版ステータスPublished - 2012 5月 15

ASJC Scopus subject areas

  • 生化学、遺伝学、分子生物学(全般)
  • 薬理学、毒性学および薬学(全般)


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