Changes and significance of Zinc finger protein A20 in mouse model of acute hepatic necrosis

[Objective] To investigate the changes and the important role of Zinc finger protein A20 in the mouse experimental hepatic necrosis model at different stages.[Methods] Acute hepatic necrosis model in mice was induced by D-galactosamine(D-GalN) and Lipopolysaccharide (LPS) complex factors. 36 Bal B/C mice were randomly divided into normal group (6 mice) and model group (30 mice). At different time point after the D-GalN/LPS injection, the liver tissues were harvested and studied with pathological observation using HE stain and the expression of A20 was detected by immunohistochemistry. [Results] A20 was not expressed in the hepatocytes of the normal group. In the model group, A20 was partly expressed 1 h after injection. The level of A20 reached peak 2 h after injection, and the Constantine score was 4.33. A20 positive hepatocytes ranged from 20%~45% and mainly located around the interlobular vein. The level of A20 decreased at 3 h, and could hardly be detected 7 h after injection. During the massive hepatocyte necrosis, A20 positive-stained hepatocytes were partly survived, but the majority of A20 negative-stained hepatocytes were destroyed. [Conclusion] A20 acts as an early endogenesis reactive factor to the inflammation. Before the massive hepatocyte necrosis, the expression of A20 increases quickly and reaches peak and then decreases. When the massive necrosis happens, the protein could hardly be detected. A20 plays an important role in inhibiting inflammatory response and protecting hepatocytes from injury.