Fig. 3

Effect of HIF-1α knockdown (KD) on lipo-apoptosis in HepG2 and Hep3B cells under hypoxia. A Western blot analysis of HIF-1α protein expression in HIF-1α KD and scramble control (SC) HepG2 and Hep3B cells under normoxia (N) and hypoxia (H) for 24 hours. B Cell death rates in KD and SC HepG2 and Hep3B cells with palmitic acid (PA) treatment at 0, 25, 50, and 100 μM concentrations under normoxia and hypoxia for 48 hours. C Western blot analysis of cleaved caspase 3 and cleaved PARP protein expression in KD and SC cells that were treated with PA at 0–100 μM concentrations under hypoxia for 48 hours. D Fatty acid β-oxidation (FAO) activity in KD and SC cells with or without 100 μM PA treatment under normoxia (DMOG-) and hypoxia mimicking (DMOG+) conditions for 12 hours. E Reactive oxygen species (ROS) levels in KD and SC cells under normoxia (N) and hypoxia (H) with PA (0–100 μM) for 48 hours. F, G Evaluation of fat deposition in KD and SC cells. Oil red staining was performed under normoxia (N) and hypoxia (H) with 50 μM PA treatment for 24 hours. Scale bars, 50 μm. Data are expressed as the mean ± standard error of the mean (SEM) (B, D, E, G). N.S.: not significant, *P < 0.05, **P < 0.01 versus control