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. 2019 Aug 6;2019:3719643. doi: 10.1155/2019/3719643

Figure 4.

Figure 4

GP increases glucose consumption in DEX-induced C2C12 myotube atrophy by AMPK/GLUT4 pathway. (a) After treatment with GP for 24 and 48 h, glucose uptake was measured by spectrophotometry. (b) After treatment with DEX for 24 and 48 h, glucose uptake was measured by spectrophotometry. ∗∗p < 0.01 versus 24 h; ## p < 0.01 vs. 48 h. (c) After treatment with DEX for 24 h, cells were incubated with GP (5–20 μg/mL) for 24 h. Glucose uptake was measured by spectrophotometry. (d) After treatment of GP for 24 h, the levels of p-AMPK/AMPK and GLUT4 in DEX-injured C2C12 myotubes were detected by Western blot analysis. (e) The relative expression of p-AMPK/AMPK was quantified by densitometry analyses. (f) The relative expression of GLUT4 was quantified by densitometry analyses. Data are expressed as the mean ± SD (n = 3); ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 compared to the control group; # p < 0.05 and ## p < 0.01 compared to the DEX group.