Montelukast prevents ischaemia/reperfusion-induced ovarian damage in rats

• DOI: 10.1016/j.ejogrb.2013.11.021
• Publication Date: 2013-12-04T15:59:18Z
• Authors: A. Akdemir; O. Erbaş; M. Ergenoğlu; A. Özgür Yeniel; F. Oltulu; A. Yavaşoğlu; D. Taskiran
• Keywords: Malondialdehyde

To investigate the efficacy of montelukast for prevention of ischaemia/reperfusion (I/R) injury in rat ovary.Twenty-four female adult rats were included in the study. I/R injury was induced by CO2 pneumoperitoneum in a laparoscopic rat model. The rats were divided at random into three groups: the sham group was subjected to catheter insertion but was not subjected to pneumoperitoneum; the saline group was subjected to 60 min of pneumoperitoneum and 30 min of reperfusion, with 1 mg/kg physiological saline administered 10 min before pneumoperitoneum; and the montelukast group was subjected to 60 min of pneumoperitoneum and 30 min of reperfusion, with 20mg/kg montelukast administered 10 min before pneumoperitoneum. Damage to ovarian tissue was scored by histopathological evaluation. Caspase-3 expression was determined immunohistochemically. Ovarian tissue levels of malondialdehyde and glutathione, and plasma total antioxidant capacity were measured biochemically.In comparison with the sham group, ovarian sections in the montelukast group had higher scores for follicular degeneration and oedema (p<0.001). Montelukast treatment prevented tissue damage in ovaries, and this result was significant. Caspase-3 expression was only observed in ovarian surface epithelium in the saline and montelukast groups. However, the mean caspase-3 expression score was higher in the saline group than the montelukast group (p<0.001). Tissue levels of malondialdehyde were higher in the montelukast group than the sham group, but plasma total antioxidant capacity and tissue levels of glutathione were significantly lower. Pretreatment with montelukast reduced lipid peroxidation (p<0.005) and improved antioxidant status in rats (p<0.001).Montelukast is effective for the prevention of I/R-induced damage in rat ovary.