The Effect of Inflammatory Cytokines in Alcoholic Liver Disease

Figure 2

The pathogenic mechanisms of alcoholic liver disease. Chronic ethanol consumption promotes the translocation of LPS from the intestine to the portal vein, where it binds to the lipopolysaccharide-binding protein (LBP). STATs induces liver regeneration. Ethanol consumption alters the intracellular balance of antioxidants with subsequent decrease in the release of mitochondrial damage, leading to hepatic apoptosis. Hepatocytes and activated Kupffer cells are suggested to be the sources of oxidative stress, which are responsible for lipid peroxidation and further apoptotic damage. Activation of hepatic stellate cells also contributes to the production of TGF-𝛽, ROS, and cytokines, leading to liver fibrosis.