Effects of carvedilol on an ischemia/reperfusion model: Biochemical, histopathological and immunohistochemical evaluation

• Published in: The journal of obstetrics and gynaecology research 2016-09, Vol.42 (9), p.1132-1140
• Main Authors: Özsoy, Asker Zeki, Nursal, Ayşe Feyda, Arıcı, Akgül, Bütün, İlknur, Uysal, Murat, Irmak Sapmaz, Hilal, Kunt İşgüder, Çiğdem, Yılmaz Doğru, Hatice, Taş, Ufuk
• Format: Article
• Language: English
• Subjects: Adrenergic alpha-1 Receptor Antagonists - administration & dosage; Animals; Apoptosis - drug effects; bcl-2-Associated X Protein - metabolism; Carbazoles - administration & dosage; Carvediol; Caspase 3 - metabolism; Disease Models, Animal; Female; Glutathione Peroxidase - metabolism; Immunohistochemistry; ischemia/reperfusion injury; Malondialdehyde - metabolism; ovarian torsion; Ovary - blood supply; Ovary - metabolism; Ovary - pathology; Propanolamines - administration & dosage; rat model; Rats; Rats, Wistar; Reactive Oxygen Species - metabolism; Reperfusion Injury - drug therapy; Reperfusion Injury - etiology; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Superoxide Dismutase - metabolism; Torsion Abnormality - complications
• ISSN: 1341-8076; 1447-0756
• DOI: 10.1111/jog.13028

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.