Skip to main content
. 2014 Sep 23;9(9):e107776. doi: 10.1371/journal.pone.0107776

Figure 6. Compound C inhibited DMH1-induced activation of Akt, increases of glucose uptake, glucose consumption, and lactic acid release.

Figure 6

(A) Western blot results showed that compound C inhibited DMH1-induced Akt activation in L6 cells. **P <0.01 vs control; ## P<0.01 vs. DMH1. (B) Compound C completely inhibited Akt activated by DMH1 in the presence of Akt inhibitor. *P<0.05 vs Akti; #P<0.05 vs Akti+DMH1. (C–E) Compound C inhibited DMH1-induced increases of glucose uptake, glucose consumption, and lactic acid release. **P<0.01 vs control. # P<0.05, ## P<0.01 vs DMH1. (F–H) Compound C alone inhibited glucose consumption, lactic acid release and p-Akt level in L6 cells. *P<0.05, **P<0.01 vs control. The concentrations of DMH1, compound C and Akti were 10 µM, 10 µM, and 0.5 µM respectively. Akti, Akt inhibitor, (1,3-Dihydro-1-(1-((4-(6-phenyl-1H -imidazo[4,5-g]quinoxalin-7-yl)phenyl)methyl)-4-piperidinyl)-2H-benzimidazol-2-one trifluoroacetate salt hydrate).