Aim: The aim of this study was to investigate the effects of carvedilol (CVD) on experimentally induced ovarian ischemia/reperfusion (I/R) injury in rats.
Methods: An ovarian I/R model was applied to rats, classified into three groups: 1 (n = 7), sham operated (control); 2 (n = 7), 3 h ischemia + 3 h reperfusion (I/R); 3 (n = 7), 3 h ischemia + CVD + 3 h reperfusion (I/R + CVD). Malondialdehyde (MDA) levels and glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities in ovarian tissues and serum were measured. Tissue damage was examined histopathologically; Bax and caspase-3 expression was determined immunhistochemically. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to show apoptotic cell death.
Results: MDA levels in ovarian tissues were significantly increased in the I/R group compared with the control. CVD administration significantly decreased tissue MDA levels in the I/R + CVD in comparison with the I/R group. GSH-Px activities in serum were higher in the I/R + CVD than in the I/R group. SOD activities in tissue and serum were significantly decreased in the I/R compared with the control group. Histological examination showed a significant improvement in ovarian morphology in the I/R + CVD compared with the I/R group. Bax and caspase-3 protein was more strongly expressed in the I/R group compared with the control and I/R + CVD groups. Apoptotic index detected by TUNEL assay was significantly increased in the I/R and decreased in the I/R + CVD group.
Conclusion: Our results suggest that CVD reduces the deleterious effects of oxidative damage on ovaries in a rat I/R model.
Keywords: Carvediol; ischemia/reperfusion injury; ovarian torsion; rat model.
© 2016 Japan Society of Obstetrics and Gynecology.