Copyright
©The Author(s) 2016.
World J Gastroenterol. Jul 7, 2016; 22(25): 5769-5779
Published online Jul 7, 2016. doi: 10.3748/wjg.v22.i25.5769
Published online Jul 7, 2016. doi: 10.3748/wjg.v22.i25.5769
Figure 3 Activation of JNK by urotensin II contributes to urotensin II-induced insulin resistance.
HepG2 cells were incubated with 100 nmol/L urotensin II (UII) for 24 h and were pretreated with the JNK inhibitor SP600125 for 30 min. Total cell lysates were analyzed by Western blot analysis. UII increased JNK phosphorylation (A), and this effect was dose-dependently abolished by SP600125 (B). The effects of UII on IRS-1 protein and glycogen content and phosphorylation of IRS-1 and GSK-3β were all rescued by SP600125 (C, D). Data from at least three independent experiments are presented as the mean ± SD. aP < 0.05 vs control group; hP < 0.05, iP < 0.001 vs insulin + UII group.
- Citation: Li YY, Shi ZM, Yu XY, Feng P, Wang XJ. Urotensin II-induced insulin resistance is mediated by NADPH oxidase-derived reactive oxygen species in HepG2 cells. World J Gastroenterol 2016; 22(25): 5769-5779
- URL: https://www.wjgnet.com/1007-9327/full/v22/i25/5769.htm
- DOI: https://dx.doi.org/10.3748/wjg.v22.i25.5769