Study on the pathogenesis of liver injury caused by alcohol and drugs.

In the present study, alcohol, lipopolysaccharide (LPS), and carbon tetrachloride (CCL) were administered to experimental mice. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 concentrations, and collagen type 1alpha (COL-1A) and fibronectin expressions were measured to evaluate pathophysiology of liver injury. Levels of ALT and AST were significantly increased by alcohol treatment. Alcohol with LPS treatment increased ALT and AST levels more than alcohol alone treatment, but it was not statistically significant. Alcohol with CCL treatment significantly increased ALT and AST levels more than alcohol alone treatment. Alcohol with LPS and CCL treatment significantly increased ALT and AST levels more than alcohol with CCL treatment. Concentrations of TNF-α, IL-1β, and IL-6 were significantly enhanced by alcohol treatment. Alcohol with LPS treatment significantly enhanced concentrations of TNF-α, IL-1β, and IL-6 more than alcohol alone treatment. Alcohol with CCL treatment significantly enhanced TNF-α, IL-1β, and IL-6 concentrations more than alcohol alone treatment. Alcohol with LPS and CCL treatment increased TNF-α, IL-1β, and IL-6 concentrations more than alcohol with CCL treatment, but it was not statistically significant. COL-1A and fibronectin expressions were significantly increased by alcohol treatment. Alcohol with LPS treatment significantly increased COL-1A and fibronectin expressions more than alcohol alone treatment. Alcohol with CCL treatment significantly increased COL-1A and fibronectin expressions more than alcohol alone treatment. Alcohol with LPS and CCL treatment increased COL-1A and fibronectin expressions more than alcohol with CCL treatment, but it was not statistically significant.