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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: MyD88 in myofibroblasts enhances nonalcoholic fatty liver disease-related hepatocarcinogenesis via promoting macrophage M2 polarization

Fig. 3

MyD88 deficiency in myofibroblasts attenuated liver inflammation and lipid metabolism-associated gene expression in HFD-induced NAFLD. A-D MyD88 fl/fl and SMA MyD88−/− mice were used for NAFLD model (n  = 5 per group), and the control group was fed with normal diet. The data are representative of at least three independent experiments. A Representative staining of F4/80, Gr1 and CD11b in liver tissues (Scale bar, 50 μm) and (B) Statistical analysis (magnification, 200×). *** p  < 0.001. C The mRNA levels of FANS2, ACC1 and SREBP1-c in the liver tissues of MyD88 fl/fl and SMA MyD88−/− mice were measured using qPCR analysis. ** p  < 0.01, *** p  < 0.001. D The protein levels of FASN, SREBP1 and SCD1 in liver tissue of MyD88 fl/fl and SMA MyD88−/− mice were determined by western blot. The densities of proteins were quantified using densitometry. Proteins were normalized to β-actin. ** p  < 0.01, *** p  < 0.001

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