Chinese Hepatolgy ›› 2025, Vol. 30 ›› Issue (1): 42-45.

• Liver Failure • Previous Articles     Next Articles

The effect of Neutrophil extracellular traps on mice with acute liver failure

YANG Shi-xin, SHI Chun-xia, GUO Jin, ZHANG, Dan-mei, WANG Yu-kun, GONG Zuo-jiong   

  1. Department of Infection, Renmin Hospital of Wuhan University, Wuhan 430060, China
  • Received:2024-04-22 Online:2025-01-31 Published:2025-03-10
  • Contact: GONG Zuo-jiong,Email: zjgong@163.com

Abstract: Objective To analyze the changes of Neutrophil extracellular traps (NETs) in liver tissue of mice with acute liver failure (ALF). To investigate the pathogenic role of NETosis in ALF liver inflammation. Methods 20 male mice were randomly divided into a normal group and a model group with 10 mice in each group. Acute hepatic failure model in mice was induced with D-galactosamine in combination with lipopolysaccharide. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBil) levels were detected in both groups of Mice. Hematoxylin-eosin (HE) staining was used to observe the pathological changes in liver. Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL) staining was used to detect hepatocyte apoptosis. Immunofluorescence staining was used to detect the expression of citline histone H3, a marker of NETs in liver. Enzyme linked immunosorbent assay (ELISA) was used to detect the level of NETs in serum and liver tissue of mice. Methods The liver structure of ALF model group was damaged, and inflammatory cell infiltration increased significantly. Serum AST, ALT and TBil levels were significantly increased (P<0.05) . NETs in the liver tissue of mice in model group (10.52±0.53 ng/mL) were significantly higher than those in normal mice (4.61±0.84 ng/mL), and the difference was statistically significant (P<0.05). Conclusion NETs play an important role in the inflammatory response of ALF. It can be used as a feasible target for the treatment of acute liver failure.

Key words: Acute liver failure, Neutrophil extracellular traps, Citrullinated histone H3