Liver regeneration post severe liver injury is crucial for the recovery of hepatic structure and function. The energy sensor AMP‑activated protein kinase (AMPK) has a crucial role in the regulation of nutrition metabolism in addition to other energy‑intensive physiological and pathophysiological processes. Cellular proliferation requires intensive energy and nutrition support, therefore the present study investigated whether AMPK is involved in liver regeneration post carbon tetrachloride (CCl4)‑induced acute hepatic injury. The experimental data indicated that phosphorylation level of AMPK increased 48 h post‑CCl4 exposure, which was accompanied with upregulation of proliferating cell nuclear antigen (PCNA) and recovery of alanine aminotransferase (ALT) level. Pretreatment with the AMPK inhibitor compound C had no obvious effects on ALT elevation in plasma and histological abnormalities in liver 24 h post CCl4 exposure. However, treatment with compound C 24 h post CCl4 exposure significantly suppressed CCl4‑induced AMPK phosphorylation, PCNA expression and ALT recovery. These data suggest that endogenous AMPK was primarily activated at the regeneration stage in mice with CCl4‑induced acute liver injury and may function as a positive regulator in liver regeneration.
Keywords: AMP-activated protein kinase; liver regeneration; energy sensor; carbon tetrachloride; acute liver injury.