Fig. 6.

Fenofibric acid treatment ameliorated the mitochondrial dysfunction induced by diabetic stressors, and enhanced proliferation and migration in HCEC. (A) The DCF fluorescence signal was measured in HCEC treated with HNE (20 µM) and fenofibric acid (FA, 20 µM) for 24 h (n = 5 to 7). (B) The DCF fluorescence signal in HCEC treated with high glucose (30 mM) and FA (20 µM) for 4 d (n = 8). (C–F) Mitochondrial stress test in HCEC treated with HNE (10 µM) and FA (20 µM) for 24 h (n = 6 to 8). (G–J) Mitochondrial stress test in HCEC exposed to high glucose (30 mM) and FA (20 µM) for 4 d (n = 6). (K) HCEC proliferation in the presence or absence of HNE (20 µM) and FA (20 µM) for 24 h was measured by Cell Proliferation BrdU ELISA (n = 3). (L) HCEC were treated with HNE (20 µM) and FA (20 µM) after 100% confluence. Images of each scratch were captured after in vitro “wound” was created at indicated time points. The acellular area was measured by ImageJ (n = 6). (M and N) HCEC proliferation (n = 5) and migration (n = 5) were measured after the cells were exposed to high glucose (30 mM) and FA (20 µM) for 4 d. Values are mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.