Skip to main content
Fig. 5 | Cell Communication and Signaling

Fig. 5

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

Fig. 5

MyD88 deficiency in myofibroblasts attenuated inflammation and fat accumulation in DEN/HFD-induced HCC. Groups of MyD88 fl/fl and SMA MyD88−/− mice (n  = 9 per group) were used for the DEN/HFD- induced liver cancer model. The data are representative of at least three independent experiments. A Representative staining of F4/80, Gr1, CD11b, CD86 and CD206 in liver tissues (Scale bar, 50 μm) and (B) Statistical analysis (magnification, 200×). * p  < 0.05, ** p  < 0.01. C-E The mRNA levels of iNOS, IL-6, MCP-1, IL-10, Arg1, YM1, SCD1 and SREBP1-c in the liver tissues of MyD88 fl/fl and SMA MyD88−/− mice were measured using qPCR analysis. * p  < 0.05, ** p  < 0.01, *** p  < 0.001. F The protein levels of FASN, SREBP1 and SCD1 in liver tissues 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  < 0.001

Back to article page