Figure 2 Pharmacological inhibition of c‐jun (NH2) terminal kinase (JNK) activity in vivo markedly reduces mortality in a mouse model of paracetamol‐induced acute liver failure. Mice were injected intraperitoneally (IP) with vehicle control or SP600125 (30 mg/kg) 1 h before IP injection with paracetamol solution (350 mg/kg). (A) Hepatic phospho‐JNK (P‐JNK) expression in the vehicle control group 2 h after paracetamol administration. (B) Hepatic P‐JNK expression in the SP600125 group 2 h after paracetamol administration. (C) Time course of hepatic JNK activity in mice injected IP with vehicle control or SP600125 (30 mg/kg) 1 h before paracetamol administration (350 mg/kg). (D) Time course of hepatic P‐JNK and phospho‐p38 in mice injected IP with vehicle control or SP600125 (30 mg/kg) 1 h before paracetamol administration (350 mg/kg). (E) Mortality at 72 h in mice injected IP with vehicle control, SP600125 (30 mg/kg) or d‐JNKI1 (c‐Jun N‐terminal kinase peptide inhibitor 1, d‐stereoisomer; 30 μg/mouse) 1 h before paracetamol administration (450 mg/kg; n = 10 mice in each group). (F) Sickness scores at 24 h in mice injected IP with vehicle control, SP600125 (30 mg/kg) or d‐JNKI1 (30 μg/mouse) 1 h before paracetamol administration (350 mg/kg; n = 10 mice in each group). Each point represents an individual mouse.