Butin prevent liver damage triggered by D-galactosamine via regulating lipid peroxidation and proinflammatory cytokines in rodents

Objectives: Liver damage is becoming a more severe problem around the world. Unfortunately, there is still a great need for clinically effective pharmacological therapy for liver injury. The investigation aimed to assess the favorable outcome of butin hepatoprotective efficacy against D-galactosamine (D-GalN)-produced liver damage in experimental rats. Methods: A single dose of D-GalN 400 mg/kg b. wt. was injected intraperitoneally, 24 hr prior to scarification of rats to cause liver damage. The liver injury was assessed biochemically, investigating parameters like aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), γ-glutamyl transferase (GGT), total-bilirubin, -albumin and -protein. Butin (25 and 50 mg/kg b. wt.) was managed for 21^st days and at the end of the experimental period, normal control, D-GalN control, and butin treatment group rats for further biochemical as well as histopathological consideration. Results: Butin pretreatment significantly attenuated D-GalN-induced hepatocytes damage by reducing hepatic markers and its ability in attenuating oxidative damage (MDA, GSH, SOD, CAT) and pro-inflammatory cytokine (TNF-α, IL-6, IL-1β) and MPO. Histopathological assessment of the liver and biochemical estimation confirmed the hepatoprotective effects of butin. Conclusions: These results demonstrated that butin protects experimental rats against D-GalN-induced liver injury by modulating lipid peroxidation and pro-inflammatory cytokine. Current research will give preliminary experimental evidence for butin, and possible therapeutic effects in liver disorders.