Fig. 5

AMPK activation counteracts hepatic cholesterol deposition and MST1 deficiency-induced hepatotoxicity. MST1-deficient murine models receiving NCD/WD regimens for 16 weeks underwent subsequent 14-day AICAR administration via intraperitoneal route. a Serum lipid profiles including TC, LDL-C, and HDL-C concentrations. b Hepatic quantification of TC and FC levels. c Histopathological characterization through Filipin-stained fluorescence microscopy (100x), F4/80 + macrophage infiltration, hematoxylin–eosin stained parenchyma, and collagen deposition visualized by Masson’s trichrome (200x), with quantitative morphometric analysis of fluorescence intensity, macrophage distribution area, fibrotic content, and NAFLD pathological scoring. d Transcriptional activation profiles of inflammatory mediators and fibrogenesis markers in hepatic tissue. e Immunoblot analysis with densitometric quantification of AMPK phosphorylation status, SREBP2 proteolytic processing, and MST1 expression in NCD-fed murine livers. f mRNA profiling of AMPK signaling components and cholesterol biosynthesis enzymes in NCD-treated hepatic samples. g Immunoblot densitometry illustrating AMPK pathway activation dynamics and SREBP2 maturation in WD-exposed liver specimens. h WD-challenged hepatic transcriptome alterations in cholesterol regulatory network components. Data expressed as mean ± SEM from sextuplicate biological replicates across three experimental iterations* versus respective controls. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001