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Fig. 4 | Nutrition & Metabolism

Fig. 4

From: High-density lipoprotein ameliorates palmitic acid-induced lipotoxicity and oxidative dysfunction in H9c2 cardiomyoblast cells via ROS suppression

Fig. 4

HDL stabilized on mitochondrial transmembrane permeability transition (Ψm) and downregulated PA-triggered mitochondrial dependent pathway, JNK phosphorylation and NFκB activity in H9c2 cells. a Cells were incubated with HDL 100 μg/ml for 2 h and then incubated with 0.5 mM PA for an additional 24 h. The change in mitochondrial membrane poteneial was assessed based on the signal intensity from monomeric (green) and J-aggregate (red) JC-1 fluorescence. No treatment (left); PA (middle); and PA + HDL (right). b H9c2 cells were pretreated with the indicated concentrations of HDL (25-100 μg/ml) for 2 h followed by PA (0.5 mM) treatment for 24 h. p-Akt, Bcl2, Bax, Caspase 3 expression was estimated by immunoblotting. c p-JNK, p-NFκB, MMP3, COX2 was estimated by immunoblotting. d Cells were transfected with a luciferase NFκB reporter construct. After transfection and treatment with PA and indicated concentrations of HDL (25-100 μg/ml), the cells were assayed for luciferase activity. Data showed the means±SEM of 3 independent analyses. # p < 0.05 vs. control; *p < 0.05 and **p < 0.01vs. palmitic acid alone treatment

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