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Fig. 3 | Skeletal Muscle

Fig. 3

From: Aminoguanidine hemisulfate improves mitochondrial autophagy, oxidative stress, and muscle force in Duchenne muscular dystrophy via the AKT/FOXO1 pathway in mdx mice

Fig. 3

AGH treatment reduced ROS. TA muscles from WT, mdx, and AGH-treatment mdx mice were isolated at 8 weeks of age. (A–B) Representative immunofluorescence images and quantification of DHE staining (red), and DAPI (blue, 20× magnification, scale bar = 50 μm). (C) Quantification of fluorescence intensity of DCF in fresh TA muscle by enzyme labeling. (D-E) Representative immunofluorescence images and quantification of MitoSOX staining (red), and DAPI (blue, 20× magnification, scale bar = 50 μm). (F–G) Representative blots and quantification for Prdx3 and MnSOD.Quantitatifications were normalized to β-tubulin level. Gene expression levels of (H) Prdx3 and MnSOD were measured using real-time PCR. Values were normalized to 36B4 for each target. (I) The activity of MnSOD in TA muscle was measured per assay kit instructions. Representative immunofluorescence images and quantification for (J–K) Prdx3 (red), wheat germ agglutinin (WGA, green), and DAPI (blue, 20× magnification, scale bar = 100 μm). Values are presented as the mean ± standard error of the mean for each experiment (n = 5). * p < 0.05 compared with WT control, # p < 0.05 compared with mdx

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