Gul, MehmetKayhan, BasakElbe, HulyaDogan, ZumrutOtlu, Ali2024-08-042024-08-0420150191-3123https://doi.org/10.3109/01913123.2013.829150https://hdl.handle.net/11616/96663Inflammation in the liver is an extraintestinal manifestation that is frequently seen during inflammatory bowel diseases (IBD). The authors investigated histopathologycal, ultrastructural and antioxidant effects of dexmedetomidine (Dex) on liver during trinitrobenzene sulfonic acid (TNBS)-induced inflammatory bowel disease. Thirty-two BALB/c mice were divided (n = 8) as follows: control; Dex (dexmedetomidine) (30 mu g/kg) for 6 days; TNBS 150 mu L, TNBS_ethanol (50% w/v) intrarectally; TNBS_Dex. The histopathological and ultrastructural changes were evaluated. The levels of malondialdehyde (MDA), activity of antioxidant enzymes (GPx and SOD) were measured in liver tissue. Induction of colitis induced histopathological and ultrastructural changes of damage in liver. Those changes were markedly reduced in the TNBS_Dex group and that reduction was even significant in comparison to the TNBS group. MDA levels were significantly higher in the TNBS group and dexmedetomidine significantly elevated SOD levels in the TNBS_Dex group. These results suggest that the administration of dexmedetomidine reduces the histopathological and ultrastructural damage and increases the defense capacity against oxidative damage on liver in this IBD mice model.eninfo:eu-repo/semantics/closedAccessDexmedetomidineelectron microscopyinflammationinflammatory bowel diseaseliveroxidative stressArticle3916122413466010.3109/01913123.2013.8291502-s2.0-84921729896N/AWOS:000348916000002Q4