Fig. 8.

Rosiglitazone reversed inhibitions of mitochondrial function and biogenesis as well as their regulation disorders in cardiomyocytes incubated with ADMA. ATP content was measured to reflect mitochondrial function (Panel a), and the ratio of the DNA copy number of COX Ι and β-actin genes was used to evaluate mitochondrial biogenesis (mtDNA, Panel b); Transcriptions (mRNA, Panel c) and expression (Protein, Panel d) of PGC-1α and UCP2 genes were detected to assess regulations of mitochondrial biogenesis and function; manganese superoxide dismutase (Mn-SOD) activity and malonyldialdehyde (MDA) content were measured to estimate oxidative stress (Pane e & f) in cardiomyocytes incubated without and with asymmetric dimethylarginine (ADMA, 30 μM) or high glucose (30 mM) or oleic acid (OA, 100 μM) for 48 h, and plus rosiglitazone (RSG, 1 μM) pretreatment for 2 h and then co-incubated with ADMA or high glucose or OA for 48 h, respectively. Graphs in panel b, c & d represent the quantifications of COX Ι vs β-actin (mtDNA), PGC-1α and UCP2 vs GAPDH (mRNA) or vs β-actin (Protein) from 3 independent experiments, respectively. Date are expressed as mean ± S.E.M., n = 3, ^**P < 0.01 vs control, ^#P < 0.05, ^##P < 0.01 vs glucose, OA or ADMA