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. 2016 Jun 9;6:27849. doi: 10.1038/srep27849

Figure 3. UFAs-induced lipid accumulation was prevented by TLR7, followed by autophagy activation.

Figure 3

Hepatocytes and TLR7KO hepatocytes were treated with or without 50 μM rapamycin, 10 mM 3-MA, and 10 μg/ml imiquimod in presence or absence of 10 mM UFAs for 72 h. (A) Oil Red O staining was performed to evaluate lipid accumulation. The red-stained areas indicated lipid droplets, which were quantified by absorbance measurement. (B) Gene expression of IGF-1 in cells was examined by real-time RT-PCR. (C) We performed immunoblotting to evaluate the protein expression of LC3A/B and IGF-1. (D) Medium from the cell supernatant was used to evaluate IGF-1 contents on ELISA. (E) ROS production was examined in cells. (F) MDA production and (G) 4-HNE production in cells were examined by ELISA. Data are mean and SEM values (n = 3). *p < 0.05 vs. untreated control. **p < 0.01 vs. untreated control. ***p < 0.001 vs. untreated control. #p < 0.05 vs. UFAs group. ##p < 0.01 vs. UFAs group. ###p < 0.001 vs. UFAs group. +p < 0.05 vs. 3-MA + UFAs group. ++p < 0.01 vs. 3-MA + UFAs group. +++p < 0.001 vs. 3-M0041 + UFAs group. $p < 0.05 vs. TLR7KO + UFAs group. $$p < 0.01 vs. TLR7KO + UFAs group. $$$p < 0.001 vs. TLR7KO + UFAs group.