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. 2018 Jun 25;9:1457. doi: 10.3389/fimmu.2018.01457

Figure 1.

Figure 1

Characterization of liver damage in lupus disease. (A) Clinical information in the cohort of 404 systemic lupus erythematosus (SLE) inpatients was reviewed and liver dysfunction (LD) was detected in 91 out of 404 SLE inpatients, while the other 313 SLE inpatients without LD served as the control group (normal liver function group). Serum biochemical markers of LD in 91 SLE patients are shown. (B) Histopathological examination of the liver and incidence of hepatic inflammation from lupus-prone mice MRL/lpr (n = 7, 22 weeks), B6 lpr (n = 10, 30 weeks), and B6 mice (n = 10, 30 weeks). Infiltration of inflammatory cells around the portal vein in these two mice models with different genetic backgrounds. The arrow indicates ballooning degeneration of hepatocytes that was observed in ~5% of the portal area. Original magnification, 100×. (C) Serum levels of liver enzymes in B6.MRL/lpr (B6 lpr) mice at various ages. ALT, alanine aminotransferase; AST, aspartate aminotransferase (n = 10). (D) Analysis of apoptosis of liver cells from B6 lpr mice (30 weeks) and age-matched control B6 mice. ***P < 0.001 (the result is representative of three independent experiments, n = 4 mice per group/experiment.) (E) Representative photomicrographs of the TUNEL in situ assay of liver sections of B6 lpr mice (30 weeks) with hematoxylin as a counter-stain. Original magnification, 400×.