Effects of rotenone on inducible nitric oxide synthase and cyclooxygenase-2 mRNA levels detected by real-time PCR in a rat bladder ischemia/reperfusion model

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Nergiz I., Baseskoglu B., YENİLMEZ A., ERKASAP N., Can C., TOSUN M.

EXPERIMENTAL AND THERAPEUTIC MEDICINE, vol.4, no.2, pp.344-348, 2012 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 4 Issue: 2
  • Publication Date: 2012
  • Doi Number: 10.3892/etm.2012.596
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.344-348
  • Keywords: rotenone, bladder, rat, ischemia/reperfusion, inducible nitric oxide synthase, cyclooxygenase-2, ISCHEMIA-REPERFUSION, EXPRESSION, INJURY, APOPTOSIS, INHIBITOR, HYPOXIA, COX-1
  • Eskisehir Osmangazi University Affiliated: Yes


We aimed to determine whether rotenone treatment prevents induced ischemia/reperfusion (I/R) damage in rat bladders by detecting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) levels by real-time PCR (RT-PCR). A total of 18 Sprague-Dawley albino rats were used in this experiment. The experimental groups each consisted of 6 rats and were treated as follows: group I, control; group II, I/R; group III, rotenone + I/R. In the control group, the rat bladders were removed by lower abdominal incision without any procedure. In the I/R group, 1 h prior to the ischemia 1 cc physiological serum was administered and the abdominal aortas were clamped for 1 h to achieve bladder ischemia. Following the ischemia, reperfusion was induced for 1 h and the bladders were removed. In the rotenone + I/R group, the rats were treated with 25 mg/kg rotenone intraperitoneally. The iNOS and COX-2 mRNA levels in each group were detected using RT-PCR. In the I/R group, the COX-2 levels in the bladder tissue were higher compared with the control group (P<0.05). The COX-2 levels in the rotenone-treated group were statistically lower compared with the I/R group (P<0.01). Vascularization and edema were markedly increased in the I/R group. Following rotenone treatment these were abrogated inversely to inflammation. Although iNOS levels were slightly higher in the I/R group compared with the control group, iNOS levels did not decrease and no significant difference was observed between the groups with regard to rotenone treatment (P>0.05). We suggest that rotenone may be used clinically to treat I/R damage due to its diminishing effect on COX-2 levels.