The Effects of Dexmedetomidine on Abdominal Aortic Occlusion-Induced Ovarian Injury via Oxidative Stress and Apoptosis

Ischemia/reperfusion (IR) induced ovarian damage is caused by various diseases such as ovarian torsion, ovarian transplantation, cardiovascular surgery, sepsis, or intra-abdominal surgery. I/R-related oxidative damage can impair ovarian functions, from oocyte maturation to fertilization. This study investigated the effects of Dexmedetomidine (DEX), which has been shown to exhibit antiapoptotic, anti-inflammatory and antioxidant effects, on ovarian ischemia-reperfusion (I/R) injury. We designed four study groups. Group 1 (n = 6): Control group; group 2 (n = 6): Only DEX group; group 3 (n = 6): I/R group, group 4 (n = 6): I/R + DEX group. Then, ovarian samples were taken and examined histologically and immunohistochemically, and tissue malondialdehyde (MDA) and glutathione (GSH ) levels were measured. In the I/R group MDA levels, caspase-3, NF-k & beta;/p65, 8-OHdG positivity, and follicular degeneration, edema, and inflammation were increased than in the Control group (P=0.000). In addition, GSH levels were significantly decreased in the I/R group compared to the Control group (P=0.000). On the other hand, in the I/R+DEX treatment group MDA levels, caspase-3, NF-k & beta;/p65, 8-OHdG positivity, follicular degeneration, edema, and inflammation findings were decreased than in the I/R group (P=0.000, P=0.005, P=0.005, P=0.001, P=0.005, respectively). However, GSH levels increased significantly in the I/R+DEX treatment group compared to the I/R group (P=0.000). DEX protects against ovarian I/R injury through antioxidation and by suppressing inflammation and apoptosis.