Figure 6.

Inhibition of DHFR attenuated the effects of PPARδ on endothelium‐dependent relaxation. C57BL/6J mouse thoracic artery rings were incubated with GW501516 (1 μmol·L⁻¹) and PA (300 μmol·L⁻¹) for 48 hr. (a) ACh‐induced vasodilator responses and (b) SNP‐induced endothelium‐independent dilation were measured (n = 5). (c) Thoracic aortic rings were isolated from Ppard WT littermates or Ppard ^EC−/− mice, with GW501516 and PA treatment for 48 hr; ACh‐induced vasodilator responses were measured (n = 5). (d) After transfection with DHFR siRNA or Scr siRNA with Lipofectamine RNAi MAX for 24 hr, mouse thoracic aortae RNA was isolated, and DHFR mRNA level was assessed by quantitative RT‐PCR (n = 5). *P < .05 versus Scr siRNA. (e) After being transfected with DHFR siRNA, mouse thoracic aortae were coincubated with GW501516 (1 μmol·L⁻¹) and PA (300 μmol·L⁻¹) for 48 hr; ACh‐induced vasodilator responses were measured (n = 5). (f) Mouse thoracic aortae were preincubated with MTX (2 μmol·L⁻¹, 1 hr) before the exposure to GW501516 (1 μmol·L⁻¹) and PA (300 μmol·L⁻¹) for 48 hr. Then ACh‐induced vasodilation was measured (n = 5). Results are shown as mean ± SEM. *P < .05 versus vehicle; ^# P < .05 versus PA; ^† P < .05 versus GW501516 + PA