Fig. 2: Quintuple deletion of Serpina1a–e exacerbates MASH progression with increased hepatic inflammation and fibrosis.
From: A1AT dysregulation of metabolically stressed hepatocytes by Kupffer cells drives MASH and fibrosis
a, Serum A1AT protein levels in A1AT KO and WT mice. b, Serum PR3 levels in NCD-fed WT (n = 5), NCD-fed A1AT KO (n = 5), FFD-fed WT (n = 10) and FFD-fed A1AT KO (n = 10) mice. c, Hepatic tissue mRNA expression of Prtn3 in each group. d–i, BW (d), LW (e), LBW ratio (f) and serum levels of ALT (g), AST (h) and cholesterol (i) in each group. j, Representative images of freshly collected liver tissues and H&E-stained liver sections from each group. k, Representative immunohistochemical staining of CLEC4F-positive KCs in liver tissue sections from each group. Quantification of the CLEC4F-positive area relative to that of WT control mice in both the NCD and FFD groups. l, Relative mRNA expression of proinflammatory genes in hepatic tissues from each group. m, Relative mRNA expression of profibrogenic genes in hepatic tissues from each group. n, Representative images of Sirius red-stained liver tissue sections from each group. The data are presented as the means ± s.d., n ≥ 5; *,#P < 0.05, **,##P < 0.01; ***,###P < 0.001 and ****,####P < 0.0001 versus the control model. ns, not significant.
