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

In the present study, alcohol, lipopolysaccharide (LPS), and carbon tetrachloride (CCL4) 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 CCL4 treatment significantly increased ALT and AST levels more than alcohol alone treatment. Alcohol with LPS and CCL4 treatment significantly increased ALT and AST levels more than alcohol with CCL4 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 CCL4 treatment significantly enhanced TNF-α, IL-1β, and IL-6 concentrations more than alcohol alone treatment. Alcohol with LPS and CCL4 treatment increased TNF-α, IL-1β, and IL-6 concentrations more than alcohol with CCL4 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 CCL4 treatment significantly increased COL-1A and fibronectin expressions more than alcohol alone treatment. Alcohol with LPS and CCL4 treatment increased COL-1A and fibronectin expressions more than alcohol with CCL4 treatment, but it was not statistically significant.