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. 2019 May 22;10:566. doi: 10.3389/fphar.2019.00566

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Copyright © 2019 Shao, Gong, Qi, Wang and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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PF inhibited the activation of TLR4 and its downstream signaling pathway in HG-induced BMDMs. (A) Densitometric analyses of the protein levels of TLR4, MyD88, p-IRAK1, Trif, p-IRF3 and IRF3 in HG-treated BMDMs. (B) Densitometric analyses of the protein levels of NF-κB p-p65, and NF-κB p65 in HG-treated BMDMs. All data were normalized to the β-actin level and are expressed as the mean ± SD from at least three independent experiments. NS: not significant; ^∗P < 0.05 and ^∗∗P < 0.01 vs. the LG group; ^#p < 0.05 and ^##p < 0.01 vs. the HG group; ^▲P < 0.05 and ^▲▲P < 0.01 vs. the TLR4-/-+HG group. Lanes: 1, LG; 2, LG+PF; 3, HG; 4, HG+PF; 5, TLR4-/-; 6, TLR4-/-+HG; and 7, TLR4-/-+HG+PF.