FIGURE 8.

PPARγ knockdown exaggerates whereas PPARγ activation ameliorates CSE-induced inflammatory response in HBE cells. A–G, effects of PPARγ knockdown with siRNA (A, C, and D) and activation with OA-NO₂ (100 nm) or Rosi (1 μm) (B and E–G) followed by CSE treatment (10%, 6 h) in normal HBE cells. A and B, Western blots showing whole-cell PPARγ levels following knockdown (A) and agonist treatment (without CSE treatment) (B). Veh, vehicle. C, deacetylase activity of HDAC (left) and DNA binding activity of NF-κB (right) measured using ELISA-based assays. D, secretion of IL-8. E, Western blots showing nuclear localization of PPARγ, GR-α, HDAC2, and NF-κB p65. F, chromatin was cross-linked and immunoprecipitated with antibodies against p65. Antibody-bound protein-DNA complexes were eluted and subjected to real-time PCR with specific primers for IL-8 and α-satellite. G, secretion of IL-8. Data are representative of three independent experiments with n = 3–5. **, p < 0.01, ***, p < 0.001, n.s. = nonsignificant.