Fig. 4
LLL exposure mitigates Dox-reduced SIRT1 and PGC-1α expression via modulation of AMPK. C2C12 cells were exposed to LLL 8J/m2 for 2 h and incubated in the 37 °C incubator with 5% CO2 for additional 22 h. The expression level of SIRT1, PGC-1α, and β-actin were investigated using Western blot assay (A). Protein expression levels were quantified and presented by a bar chart (B, C). C2C12 cells were treated with 2 µM doxorubicin (Dox) for a total of 24 h, in the LLL-treated group, cells were exposed to LLL 8 J/m2 before Dox treatment. The expression level of SIRT1, PGC-1α, and β-actin were investigated using Western blot assay (D). Protein expression levels were quantified and presented by a bar chart (E, F). In the LLL-treated group, cells were exposed to LLL 8J/m2 for 2 h before Dox treatment. In LLL plus AMPK silencing group, cells were transfected with AMPK siRNA for 36 h before LLL exposure and Dox treatment. The expression level of SIRT1, PGC-1α, and β-actin were investigated using Western blot assay (G). Protein expression levels were quantified and presented by a bar chart (H, I). Western blot analysis of phosphorylated AMPK, SIRT1, and PGC-1α in the left soleus muscle from after LLL intervention without Dox injection (J). Bar graphs illustrate densitometric analyses of phosphorylated AMPK, SIRT1, and PGC-1α expression levels (K). Western blot analysis of phosphorylated AMPK, SIRT1, and PGC-1α in the left soleus muscle (L). Bar graphs illustrate densitometric analyses of phosphorylated AMPK, SIRT1, and PGC-1α expression levels (M). The data were presented as the mean ± SD of three biological replicates at three separate times. (* indicating p < 0.05 compared with the control group; # indicating p < 0.05 compared to Dox group; & indicating p < 0.05 compared to only LLL exposure group)