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Fig. 5 | Cell & Bioscience

Fig. 5

From: Low-level laser prevents doxorubicin-induced skeletal muscle atrophy by modulating AMPK/SIRT1/PCG-1α-mediated mitochondrial function, apoptosis and up-regulation of pro-inflammatory responses

Fig. 5

LLL exposure protects against Dox-impaired mitochondria function and biogenesis. 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 mitochondrial membrane potential was investigated by JC-1. Results of JC-1 were obtained by a fluorescence microscope (A) and flow cytometry (B). FL-1 (green) and FL-2 (red) from the flow cytometry were quantified and presented by a bar chart (C). The mitochondrial oxygen consumption rate (ORC) was investigated by the Seahorse analyzer (D). The mt DNA copy number, which represents the biogenesis of mitochondrial, was investigated by the real-time PCR (E). The mitochondria superoxide was tested using the MitoSOX (F). Cytosolic ROS was investigated by DCF-DA (G). 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)

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