Cellular changes post hepatectomy in cirrhotic vs normal rats

Abstract

Hepatectomy is the only treatment that has the potential to cure liver cancer. Most liver cancer develops in a cirrhotic liver. Although normal liver has a remarkable capacity to regenerate, the regeneration of cirrhotic liver is delayed. As the demand of energy increases for liver regeneration, mitochondria must play an important role. Many cytokines and growth factors also play important roles in liver regeneration. After hepatectomy, most hepatocytes enter into the cell cycle from the quiescent state. In this study, decreased mitochondrial GSH level and glutathione peroxidase activity resulted in higher level of lipid peroxidation. There were also decreased NADH-cytochrome c reductase activity, succinate-cytochrome c activity and respiratory control ratio post-hepatectomy in cirrhotic liver. Decreased TNF-I?, IL-6, cyclin D1, D3, E, A and cdk4, 2 expressions and upregulated p21 and p27 levels may also contribute to the delayed regeneration in cirrhotic liver after hepatectomy.