Fig. 6
LLL exposure reduces Dox-caused proinflammatory responses by regulating AMPK/SIRT1/PGC-1a-mediated mitochondria function. 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. In LLL plus AMPK, SIRT1, and PGC-1α silencing groups, cells were transfected with AMPK or SIRT1 or PGC-1α siRNA for 36 h before LLL exposure and Dox treatment. The expression level of p-p38, p38, nuclear NF-κBp65, and nuclear HADC1 were investigated using Western blot assay (A). Protein expression levels were quantified and presented by a bar chart (B, C). The activity of nuclear NF-κBp65 was investigated by a commercial kit (D). IL-8, Atrogin-1, and MuRF-1 mRNA expression levels were investigated by the real-time PCR. 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)