system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Actins, Analysis of Variance, Animals, Cell Movement, Cells, Cultured, Collagen Type I, Cyclooxygenase 2, Deoxyguanosine, Gene Expression, Hepatic Stellate Cells, Imidazoles, Inflammation, Liver Cirrhosis, Male, Membrane Proteins, Mice, NF-kappa B, Nerve Tissue Proteins, Oxidative Stress, Superoxide Dismutase, Thioacetamide, Up-Regulation.
user
Does imidazolium salt attenuate thioacetamide-induced liver fibrosis in mice by modulating inflammation and oxidative stress? Context: Oxidative stress contributes to liver fibrosis through the activation of hepatic stellate cells. In a cell-based screening study, a class of imidazolium salts demonstrates anti-fibrogenic properties. Little is known on imidazolium salt mechanistic effects. We investigated the anti-fibrogenic effect of one of the imidazolium salts, 1,3-bisbenzylimidazoliumbromide (DBZIM), in a chronic mouse model of liver fibrosis and evaluated the mechanism of this treatment. Liver fibrosis was induced in mice by oral feeding of thioacetamide for 16 weeks. DBZIM was administered weekly, starting on the first day or 12 weeks from the day of thioacetamide administration. Hepatic function, histology and oxidative stress were examined. Expression of key inflammatory molecules and the molecular mechanism of DBZIM were assessed in hepatic stellate cells. DBZIM decreased the fibrogenic response in thioacetamide-mice as measured by collagen deposition and α-smooth muscle actin expression (P<0.01). DBZIM improved liver function and reduced both oxidative damage and inflammation (P<0.01). Most importantly, our findings report the discovery that astrocyte elevated gene-1, involved in tumour progression, was up-regulated in thioacetamide-mice and DBZIM modulated astrocyte elevated gene-1 and NF-κB expression.
assistant
These findings indicate DBZIM is a potent therapeutic agent for the treatment of liver fibrosis. Final Decision: yes