Demirel, UlviHarputluoglu, Murat M. M.Seckin, YukselCiralik, HarunTemel, IsmailOzyalin, FatmaOtlu, Baris2024-08-042024-08-0420110960-32711477-0903https://doi.org/10.1177/0960327110374206https://hdl.handle.net/11616/95365Tumor necrosis factor (TNF)-alpha antibodies have been shown to reduce liver damage in different models. We investigated the effects of infliximab (a TNF-alpha antibody) on liver damage in thioacetamide (TAA)-induced hepatotoxicity in rats. Group 1 (n = 8) was the control group. In group 2 (n = 8), the TAA group, the rats received 300 mg/kg intraperitoneal (ip) TAA daily for 2 days. In group 3 (n = 8), the TAA + Infliximab (INF) group, infliximab (5 mg/kg ip daily) was administered 48 hours before the first dose of TAA daily for 2 days and was maintained for 4 consecutive days. In group 4 (n = 8), the INF group, the rats received only ip infliximab (5 mg/kg) daily. Livers were excised for histopathological and biochemical tests (thiobarbituric-acid-reactive substances [TBARS], and myeloperoxidase [MPO]). Serum ammonia, aspartate transaminase (AST), alanine transaminase (ALT), TNF-alpha, liver TBARS and MPO levels, and liver necrosis and inflammation scores in the TAA group were significantly higher than in the control and INF groups (all p < 0.01). All parameters except AST were not significantly different between TAA and TAA + INF. In conclusion, our results suggest that oxidative stress plays an important role in TAA-induced hepatotoxicity, and infliximab does not improve oxidative liver damage.eninfo:eu-repo/semantics/closedAccessinfliximabtumor necrosis factor-alphathioacetamideoxidative stressliverArticle3075605662053463810.1177/09603271103742062-s2.0-79959728232Q2WOS:000291891200006Q3