Figure 4
MyD88 is required for PM2.5-triggered hepatic autophagy and its counteractive effect on hepatic steatosis. (A) Western blot analyses of levels of LC3, P62, MyD88, and β-actin in the liver tissues of NC-fed WT or MyD88 KO mice exposed to PM2.5 or FA for 10 weeks. Liver protein lysates were prepared from pooled liver tissues of each group of mice (n = 4 mice per group). The graphs beside the images show the quantitative analyses of fold changes of ratios of LC3-II vs LC3-I and P62 protein levels, as determined by Western blot densitometry, in the livers of NC- or HFD- fed mice exposed to PM2.5 or FA. The protein level was normalized to that of β-actin before fold change calculations. (B) Expression levels of Lc3b, P62, Tfeb, Psap, Gba, and Csta mRNAs in the livers of the PM2.5- or FA- exposed WT and MyD88 KO mice under NC or HFD. Expression levels of mRNAs were determined by qPCR. Fold changes of mRNA levels are shown by comparing to that of one of NC-fed mice under FA exposure. Each bar denotes mean ± SEM (n = 4 mice per group). *p < 0.05, **p < 0.01. (C–D) Oil-red O staining of lipid droplets in the livers of NC- or HFD- fed WT and MyD88 KO mice exposed to PM2.5 or FA for 10 weeks (magnification: 200×). (E–F) Levels of hepatic TG in the liver tissues of NC- or HFD- fed WT and MyD88 KO mice exposed to PM2.5 or FA for 10 weeks. N = 4–6 mice per group. Each bar denotes mean ± SD. *p < 0.05.
