Myeloperoxidase, extracellular DNA and neutrophil extracellular trap formation in the animal models of metabolic dysfunction-associated steatotic liver disease

Figure 4 Choline-deficient L-amino acid-defined diet-induced model liver damage-associated and metabolic parameters. A: Experimental design; B: Dynamics of body weight; C: Dynamics of cumulative caloric intake; D: Dynamics of fasting glycemia; E: Dynamics of alanine aminotransferase activity; F: Dynamics of aspartate aminotransferase activity; G: Body mass index; H: Concentrations of fasting insulin; I: Quantitative index of insulin sensitivity; J: Concentrations of cholesterol; K: Concentrations of triacylglycerols; L: Concentrations of albumin; M: Relative liver weight; N: Concentration of liver triacylglycerides; O: Concentration of liver cholesterol; P: Nonalcoholic steatohepatitis score; Q: Fibrotic score; R: Neutrophil infiltration into the liver; S: Concentration of myeloperoxidase in the liver; T: Concentration of neutrophil elastase in the liver. Data shown in G-T are after 10 weeks of the choline-deficient L-amino acid-defined (CDAA) model. Data are presented as mean ± SE. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001; B-F: Repeated two-way analysis of variance and Bonferroni post-hoc test; G-T: Independent Student’s t-test. CTRL CSAA: Control group (n = 7); CDAA: Experimental liver steatosis group (n = 10). CTRL CSAA: Choline-sufficient L-amino acid-defined control; CDAA: Choline-deficient L-amino acid-defined. MPO: Myeloperoxidase; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; BMI: Body mass index; NASH: Nonalcoholic steatohepatitis; NE: Neutrophil elastase.