LPS/D-Gal-induced liver injury in mice is a well-established experimental hepatitis model.13 The hepatocyte damage in this model largely depends on the early production of detrimental inflammatory mediators such as tumor necrosis factor alpha (TNF-α), and these deleterious factors might induce massive hepatocyte apoptosis and lethal outcomes at the late stage.14, 15 In the present study, the phosphorylation status of AMPK was determined. Here, TNF is linked to hepatitis A virus infection.