Fig. 2

MyD88 deficiency in myofibroblasts attenuated fat accumulation in HFD-induced NAFLD. MyD88 ^fl/fl and SMA ^MyD88−/− mice were fed with HFD to establish a 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 Primary hepatic stellate cells were isolated from MyD88 ^fl/fl and SMA ^MyD88−/− mice liver, immunofluorescence double staining of α-SMA (red) and MyD88 (green) in liver tissues (Scale bar, 50 μm). B The protein level of MyD88 in the primary hepatic stellate cells of MyD88 ^fl/fl and SMA ^MyD88−/− mice were measured using western blot. C Body weight at end of diet. D Representative images of the livers from SMA ^MyD88−/− mice and control mice. E Liver weight, (F) Glucose tolerance test (GTT), (G) ALT, (H) AST, (I) TG and (J) TC levels of MyD88 ^fl/fl and SMA ^MyD88−/− mice are shown. * p  < 0.05, ** p  < 0.01. *** p < 0.001. K Representative H&E, Oil red O staining and staining of α-SMA in liver tissues of MyD88 ^fl/fl and SMA ^MyD88−/− mice. Scale bar, 50 μm. Statistical analysis. ** p  < 0.01 (L-M) The protein levels of MyD88 and α-SMA 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 < 0.05, ** p < 0.01. ALT: alanine aminotransferase; AST: aspartate aminotransferase; TG: triglyceride; TC: total cholesterol