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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: IFN-γ-mediated inhibition of JAK/STAT signaling via nano-scutellarin treatment is an efficient strategy for ameliorating liver fibrosis

Fig. 1

IFN-γ plays a key regulatory role in mediating EndMT during liver fibrosis. (A) Animal experiment design flow chart. (B) Immunofluorescence staining of human liver sections from control and MASH cases was performed to visualize IFN-γ (green) and CD31 (red), while nuclei were counterstained with DAPI (blue). Scale bar, 100 μm. (C) H&E, Sirius Red, and Masson staining was performed on liver sections from MASH mice (n = 4 mice/group). Scale bar, 100 μm. (D, E) ALT or AST enzyme activities were measured in designated groups of mice (n = 4 mice/group). (F) Immunofluorescence staining of mouse liver sections for Fibronectin (green) after induction of chronic liver injury by HFD-fed (n = 4 mice/group). Scale bar, 100 μm. (G, H) Co-localization of the endothelial marker CD31 with the mesenchymal markers α-SMA and FSP1 was detected in liver sections from mice exhibiting MASH (n = 4 mice/group). Scale bar, 100 μm. Protein expressions were qualified with densitometry analysis using ImageJ. Statistical analyses were performed using GraphPad Prism 9 software and values across groups were compared using one-way ANOVA. Outliers were detected using Grubbs’ test. Data are expressed as the mean ± S.D. *p < 0.05; **p < 0.01

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