Biochemical and Histopathological Evaluation of Sunitinib Effect on Ovarian Injuries by Ischemia-Reperfusion in Rats

Background and Objective: Interleukin 1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) as the proinflammatory cytokines, whose production increases during reperfusion after ischemia (I/R), were reported to produce the Reactive Oxygen Species (ROS). It was reported that sunitinib has proinflammatory cytokine expression suppression and antioxidant effects. The study aims to investigate the effects of sunitinib on ovarian injuries created by I/R in albino Wistar female rats biochemically and histopathologically. Materials and Methods: Animals divided into 3 groups as sunitinib+ovarian tissues (SOIR), I/R ovarian tissues (OIR) and Sham operation (SG) groups. There were ischemia and reperfusion procedures for 2 hrs on the right ovaries of the OIR and SOIR group rats. Results: The Nuclear Factor kappa B (NF-kappa B), Tumour Necrosis Factor-alpha (TNF-alpha), Malondialdehyde (MDA) and Interleukin 1 beta (IL-1 beta) levels in the OIR group's ovarian tissue were high whereas their total glutathione (tGSH) level was found to be low compared to the SOIR and SG group. While distinct histopathologic injuries were seen in the ovarian tissue of the OIR group, histopathologic injuries in the SOIR group were mild. Conclusion: Sunitinib prevented the oxidant and proinflammatory cytokine increase and antioxidant decrease related to I/R. It is concluded that sunitinib might be used for the treatment of ovarian I/R injuries.