ox-LDL-Induced Endothelial Progenitor Cell Oxidative Stress via p38/Keap1/Nrf2 Pathway

Figure 3

Nrf2 mediated ox-LDL-induced EPC oxidative stress and mitochondrial dysfunction. After being pretreated with Keap1 siRNA or 1 μM SB203580, EPCs were exposed to ox-LDL (20 μg/mL) for 6 hours. The control well was treated with medium alone. Intracellular ROS levels were estimated using the probe DCFH-DA. (a) Representative images of EPCs treated by control, 20 μg/mL ox-LDL, 20 μg/mL ox-LDL plus Keap1 siRNA, and 20 μg/mL ox-LDL plus 1 μM SB203580. Scale: 100 μm. (b) Fluorescence was read at 520 nm for emission and 485 nm for excitation. Quantification of relative fluorescent intensity showed that ox-LDL-induced elevation of ROS levels in EPCs was reversed by pretreatment of Keap1 siRNA and SB203580. (c) Represent images of EPCs stained by JC-1 in each group after the treatment. Scale: 200 μm. (d) ox-LDL-induced EPC mitochondrial dysfunction which was reversed by Keap1 siRNA. vs. control. ^# vs. ox-LDL group.

(a)

(b)

(c)

(d)