The aim of this study was to investigate the effects of
urocortin (UCN) on oxidative stress and the mechanisms of
urocortin on
ischemia-reperfusion injury in vivo in the rat model. Thirty-six Sprague-Dawley rats were divided into 6 groups, including
sham, control (
normal saline solution), UCN1, UCN2, UCN3, and
verapamil groups. The left anterior descending coronary artery of all rats except those in the
sham group was treated with a 30-min occlusion followed by a 60-min reperfusion. Just before the occlusion,
normal saline solution, UCN (5, 10, and 20 microg/kg body mass), or
verapamil (1 mg/kg body mass) was administered. Heart rates, beating rhythm, and S-T segments were constantly monitored using an ECG. At the completion of the
drug administration, blood samples were taken to measure the activity of
superoxide dismutase (SOD),
malonaldehyde (MDA),
glutathione peroxidase (GSH-PX), and
nitric oxide (NO) to evaluate the effects of UCN on oxidative stress. Finally, the size of
infarction was measured.
Arrhythmia rates were significantly lower, and the
infarction size was significantly smaller (p < 0.01), in the UCN groups vs. the control group.
Verapamil also significantly reduced
arrhythmia rates and
infarction size. The MDA activities were remarkably diminished, whereas the SOD, GSH-PX, and NO activities were significantly higher in the UCN and VER groups (p < 0.01). MDA, SOD, and NO activities were strongly correlated with UCN doses. These results suggest that UCN may play a protective role in
ischemia-reperfusion injury in rat hearts against the oxidative stress by inhibiting
free radicals' activities.