A20 rescues hepatocytes from apoptosis through the NF-κB signaling pathway in rats with acute liver failure.

Acute liver failure (ALF) is a disease of acute derangements in the hepatic synthetic function with defects involving innate immune responses, which was reported to be negatively regulated by tumor necrosis factor α-induced protein 3 (A20). Herein, the present study was conducted to investigate the effects the A20 protein on the proliferation and apoptosis of hepatocytes through the nuclear factor (NF)-κB signaling pathway in the rat models simulating ALF. Male Wistar rats were used to simulate ALF in the model rats.