Figure 3
From: Metabolic remodeling agents show beneficial effects in the dystrophin- deficient mdx mouse model
Effect of GW and AICAR on mitochondrial activity. Fluorescent-activated cell scanning (FACS) of primary myoblasts isolated from untreated and drug-treated mdx mice. Representative dot plot FACS overlay of mitochondrial mass with nonyl acridine orange (NAO) staining (A and B) and staining for mitochondrial activity with 3, 3’-dihexyloxacarbocyanine iodide (DiOC6) in myoblasts derived from the muscles of treated mice (C, D). Histograms show geometric mean fluorescence of NAO and DiOC6 in dystrophin-deficient myoblasts. Quantification of mRNA expression of PGC-1 α (E), Cyt c (F) and PDK-4 (G) relative to GAPDH mRNA expression by RTqPCR in gastrocnemius with n = 2 for each group. Quantification of NADH activity in histological sections of EDL (H) and soleus (I) muscles, with immunolabeling of the soleus muscle for Type I (J) and type IIA (K) fibers. (L) EDL twitch force parameters, ratio of the maximal twitch force (Pt) to the time required to reach this force (tpt), and (M) lactate dehydrogenase activity of TA muscle. All experiments involved vehicle- (n = 8), GW- (n = 6), AICAR- (n = 8), and GW&AICAR-treated (n = 6) mice. Data are means ± SE. * P < 0.05 vs. vehicle-treated control mice. **P < 0.01 vs. vehicle-treated control mice. *** P < 0.001 vs. vehicle-treated control mice.