Figure 5 c‐Jun (NH2) terminal kinase (JNK) inhibition is not protective in acute carbon tetrachloride (CCl₄)‐ or anti‐Fas antibody‐mediated hepatic injury. CCl₄ model: mice were administered CCl₄ at a ratio of 1:3 with olive oil at a dose of 1 μl/g body weight 1 h after treatment with control, SP600125 (30 mg/kg) or d‐JNKI1 (c‐Jun N‐terminal kinase peptide inhibitor 1, d‐stereoisomer; 30 μg/mouse; n = 6 mice in each group). (A) Liver histology 24 h after CCl₄ administration. Scale bar 200 μm. (B) Hepatic necrosis scores 24 h after CCl₄ administration (p = NS). (C) Serum alanine aminotransferase (ALT) release 24 h after CCl₄‐induced liver injury (p = NS). Fas model: mice were administered anti‐Fas antibody (0.5 μg/g body weight) 1 hour after treatment with control, SP600125 (30 mg/kg) or d‐JNKI1 (30 μg/mouse; n = 6 mice in each group). (D) Liver histology 6 h after anti‐Fas antibody administration. Scale bar 200 μm. (E) Hepatic necrosis scores 6 h after anti‐Fas antibody administration (p = NS). (F) ALT release 6 h after anti‐Fas antibody‐induced liver injury (p = NS).