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Fig. 4 | Cell Communication and Signaling

Fig. 4

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

Fig. 4

MyD88 deficiency in myofibroblasts attenuated DEN/HFD-induced liver cancer. Groups of MyD88 fl/fl and SMA MyD88−/− mice were used for the DEN/HFD-induced liver cancer model (n  = 9 per group). The data are representative of at least three independent experiments. A Body weight, (B) Representative images of mouse livers, (C) Tumor incidence, (D) Liver weight, E Size of the maximal tumors and (F) Number of tumors per mouse are shown. * p  < 0.05, ** p  < 0.01. G Glucose tolerance test, serum (H) TG and (I) TC of MyD88 fl/fl and SMA MyD88−/− mice are shown. * p  < 0.05, ** p  < 0.01. J H&E, Ki67, Sirius Red and Oil red O staining and immunofluorescence staining of α-SMA and MyD88 in liver tissues of MyD88 fl/fl and SMA MyD88−/− mice. Scale bar, 50 μm. K The protein levels of MyD88 and α-SMA in liver tissues of MyD88 fl/fl and SMA MyD88−/− mice treated with DEN/HFD were determined by western blot. The densities of proteins were quantified using densitometry. Proteins were normalized to β-actin. *p<0.05, **p<0.01

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