Investigation of the effect of Dexmedetomidine (Dex) on inflammatory bowel diseases (IBD) induced renal damage by using an experimental model. IBD frequently cause reduction in renal function and renal failure. Since perioperative anesthesia and postoperative conditions in intensive care can cause acute kidney injury and reduction on renal function; deciding on a sedative and anesthetic agent without side effects would reduce IBD caused renal damage. We investigated histopathological, electron microscopic analyzes and antioxidant effects of Dex on kidney tissue during trinitrobenzene sulfonic acid (TNBS) induced damage in BALB/c mice at two different concentrations of Dex; 5Î¼g/kg and 30Î¼g/kg. Blood samples were collected to analyze creatinine levels. The levels of malondialdehyde (MDA) and activity of antioxidant enzymes glutathione (GSH) and superoxide dismutase (SOD) were measured in tissue homogenates. Histopathological and ultrastructural changes in kidney following TNBS induction were significantly reduced in Dex treatment groups. Administration of Dex significantly reduced creatinine levels. MDA levels were significantly reduced in Dex groups. Administration of Dex brought back GSH level to control level. Administration of Dex significantly 1.48 and 1.96 times increased SOD activity at 5Î¼g/kg and 30 Î¼g/kg, respectively. Dexmedetomidine treatment may have benefits to prevent IBD induced renal damage.
Dexmedetomidine, Inflammatory Bowel Diseases, Renal Damage