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. 2017 May 3;7:1397. doi: 10.1038/s41598-017-01603-9

Figure 5.

Figure 5

PDX ameliorates inflammation and insulin resistance through a PPARα-mediated pathway. (A) Western blot analysis of PPARα expression in differentiated C2C12 cells treated with PDX (0–1 μM) for 24 hr. (B) Confirmation of PPARα siRNA efficiency in differentiated C2C12 cells. Western blot analysis of palmitate (200 μM)-induced inflammation markers in PPARα siRNA (20 nM)-transfected differentiated C2C12 cells treated with PDX (0–1 μM) for 24 hr. (C) Western blot analysis of palmitate-induced impairment of IRS-1 and Akt phosphorylation in PPARα siRNA-transfected differentiated C2C12 cells treated with PDX (0–1 μM) for 24 hr. Human insulin (10 nM) was used to stimulate insulin signaling for 3 min. (D) Western blot analysis of PPARα expression in soleus muscle of mice treated HFD and PDX (five animals per treatment group). Western blot analysis of (E) AMPK phosphorylation in PPARα siRNA or (F) PPARα expression-transfected differentiated C2C12 cells treated with PDX (1 μM) for 24 hr. Means ± SEM were obtained from three separated experiments or five animals. *** P < 0.001 and * P < 0.05 when compared to the control or the ND treatment. !!! P < 0.001 and !! P < 0.01 when compared to the palmitate or the HFD treatment. ### P < 0.001 and # P < 0.05 when compared to the palmitate plus PDX treatment.