fig2

Retinoic acid-related orphan receptors regulate autophagy and cell survival in cardiac myocytes during hypoxic stress

Figure 2. Nobiletin rescues mitochondrial perturbations during hypoxia. (A) epifluorescence stinging of mitochondrial morphology aspect ratio with mitochondrial HSPD1 in cardiac myocytes under NMX and HPX conditions in the presence and absence of Nob, bar: 10 μm, histogram shows mitochondrial form factor (FF) which quantifies mitochondrial morphology as an index of mitochondrial fusion and fission. (B) green fluorescence staining of mitochondrial permeability transition pore opening (mPTP) of cardiac myocytes under normoxia (NMX) and hypoxia (HPX) in the presence and absence of Nob, bar: 20 μm; (C) red fluorescence staining of mitochondrial membrane potential (ΔΨm) by TMRM in cardiac myocytes under NMX and HPX conditions in the presence and absence of Nob, bar: 20 μm; (D) red fluorescence staining of mitochondrial reactive oxygen species (ROS) by dihydroethidine in cardiac myocytes under NMX and HPX conditions in the presence and absence of Nob, bar: 100 μm; Data are expressed as mean ± SEM. *P < 0.05; **P < 0.01, n = 3-4 independent myocyte isolations, counting > 200 cells for each condition tested.

The Journal of Cardiovascular Aging

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