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. 2018 Oct 26;9:1226. doi: 10.3389/fphar.2018.01226

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Copyright © 2018 Luo, Huang, Wang, Liu, Cai, Li and Zhou.

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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Effect of JNK inhibition on insulin signaling through IRS1/Akt/eNOS pathway in the resistin-treated HUEVCs. (A) Resistin (100 ng/mL) increased JNK phosphorylation, which was prevented by TUDCA (N = 7, per condition); (B) TUDCA (500 μg/mL) or JNK inhibitor (12.5 μmol/L) prevented resistin-induced IRS phosphorylation at serine residue (Ser 307); (C,D) JNK inhibitor Sp600125 (12.5 μmol/L) improved insulin signaling molecules pAkt (Ser 473), peNOS (Ser1177) impaired by resistin (N = 7, per condition). ^∗p < 0.05, vs. control, ^#p < 0.05, vs. correspondence resistin group, ^†p < 0.05 vs. insulin group.