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

Figure 2 Liver damage-associated and metabolic parameters for the thioacetamide-induced model. A: Experimental design; B: Dynamics of body weight; C: Dynamics of cumulative caloric intake; D: Dynamics of fasting glycemia; E: Dynamics of plasma alanine aminotransferase activity; F: Dynamics of plasma aspartate aminotransferase activity; G: Body mass index; H: Concentration of fasting insulin; I: Quantitative insulin sensitivity check index; J: Concentration of cholesterol; K: Concentrations of triacylglycerols; L: Concentrations of albumin; M: Relative liver weight; N: Concentrations of liver triacylglycerides; O: Concentrations 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 thioacetamide-induced 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. VEH: Control group of females (n = 7); TAA: Experimental liver fibrosis group of females (n = 11).