Kadıoglu, Berrin Goktug; Gundogdu, Betul; Kurt, Nezahat; Suleyman, Halis; Suleyman, Zeynep

OBJECTIVE: To examine the effect of desloratadine on ovarian ischemia-reperfusion (I/R) injury in rats by biochemical and histopathological methods. STUDY DESIGN: I/R was induced in the right ovaries after distilled water was given to a group of female albino Wistar rats in this study. 15 mg/kg desloratadine was orally administered to another group and I/R was induced in their ovaries, whereas I/R was not induced in the sham operation group. After 2 hours of ischemia and 2 hours of reperfusion, malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-κB (NF-κB), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) levels were measured in ovarian tissues extracted from the body of the animals sacrificed with a high dose of ketamine (120 mg/kg). Tissues were also evaluated histopathologically. RESULTS: It has been revealed that desloratadine significantly inhibited the increase of I/R-associated MDA, NF-κB, IL-1β, and TNF-α levels in the ovarian tissues of animals and the decrease in tGSH levels. In addition, desloratadine decreased severe I/R-associated histopathological damage. CONCLUSION: Our experimental results have shown that desloratadine is beneficial in terms of protecting ovarian tissue against I/R injury.

Kara, Ali Veysel; Aldemir, Mehmet Naci; Ozcicek, Fatih; Mammadov, Renad; Yazıcı, Gulce Naz; Sunar, Mukadder; Gulaboglu, Mine

OBJECTIVE: To show the protective effects of taxifolin on cisplatin-induced oxidative renal injury. STUDY DESIGN: Rats were divided into 3 groups: the healthy group, the cisplatin group (2.5 mg/kg cisplatin only), and the taxifolin-cisplatin group (50 mg/kg taxifolin+2.5 mg/kg cisplatin). The rats were sacrificed after 14 days, and the kidneys were removed for examination of malondialdehyde (MDA), total glutathione (tGSH), and super oxide dismutase (SOD) levels. Blood urea nitrogen (BUN) and creatinine levels were measured in the blood samples taken before the animals were sacrificed. Kidney tissues were examined histopathologically. Finally, biochemical and histopathological results of the groups were compared. RESULTS: Cisplatin significantly increased MDA and decreased tGSH and SOD in the rat kidney tissue (p<0.001). Additionally, cisplatin caused an increase in serum creatinine and BUN levels (p<0.001). Taxifolin prevented the cisplatin-induced increase in MDA and decrease in tGSH and SOD (p<0.001). It also decreased serum creatinine and BUN levels significantly as compared with the cisplatin group (p<0.001). In the cisplatin group microscopic examinations showed obvious kidney damage including dilation, severe necrosis, and degenerative changes. Taxifolin prior to cisplatin markedly ameliorated these changes. CONCLUSION: We have demonstrated for the first time that taxifolin can prevent cisplatin-induced nephrotoxicity.