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In the present study, alcohol, lipopolysaccharide (LPS), and carbon tet-rachloride (CCL4) were administered to experimental mice. Alanine ami-notransferase (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 mea-sured 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 treat-ment, 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. Concentra-tions of TNF-α, IL-1β, and IL-6 were significantly enhanced by alcohol treatment. Alcohol with LPS treatment significantly enhanced concen-trations of TNF-α, IL-1β, and IL-6 more than alcohol alone treatment. Al-cohol 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 signif-icant. COL-1A and fibronectin expressions were significantly increased by alcohol treatment. Alcohol with LPS treatment significantly in-creased 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 expres-sions more than alcohol with CCL4 treatment, but it was not statistically significant.