Figure 5.

PPARδ activation attenuated PA‐induced DHFR loss and eNOS uncoupling. (a) ECs were pretreated with GW501516 (0–1 μmol·L⁻¹, 12 hr) before the exposure to PA (200 μmol·L⁻¹, 24 hr); DHFR protein level was measured by western blotting (n = 5). (b) ECs were pretreated with GSK0660 (2 μmol·L⁻¹, 1 hr) and then incubated with GW501516 (1 μmol·L⁻¹, 12 hr) before the exposure to PA (200 μmol·L⁻¹, 24 hr); DHFR protein level was measured (n = 5). (c, d) Protein levels of eNOS dimers and monomers were detected by using low temperature SDS‐PAGE (n = 5). (e) ECs were pretreated with GW501516 (1 μmol·L⁻¹, 12 hr) before the exposure to PA (200 μmol·L⁻¹, 24 hr). Production of ROS was measured with L‐012 chemiluminescence in the absence or presence of L‐NAME (100 μmol·L⁻¹, n = 5). (f) Superoxide production was measured with DHE‐HPLC (n = 5). Data are shown as mean ± SEM. *P < .05 versus vehicle; ^# P < .05 versus PA; ^† P < .05 versus PA + GW501516