PHI treatment activates PPARγ signaling by downregulating MMP8 expression. (A and B) Following MMP8 overexpression, the induction of cell apoptosis of LPS-treated BEAS-2B cells, which were pretreated with PHI, was assessed using a TUNEL assay (magnification, ×200; scale bar, 100 µm). ***P<0.001 vs. control; ###P<0.001 vs. LPS group; ∆∆∆P<0.001 vs. LPS + PHI group. (C) Western blotting was used to determine the expression levels of the apoptosis-associated proteins in LPS-induced BEAS-2B cells treated with PHI and transfected with pcDNA3.1-MMP8. ***P<0.001 vs. control; ##P<0.01, ###P<0.001 vs. LPS group; ∆∆P<0.01 vs. LPS + PHI group. (D) Western blotting was used to determine the expression levels of PPARγ in LPS-induced BEAS-2B cells treated with PHI and transfected with pcDNA3.1-MMP8. ***P<0.001 vs. control; ###P<0.001 vs. LPS group. PHI, phillygenin; PPARγ, peroxisome proliferator-activated receptor γ; LPS, lipopolysaccharide; NC, negative control; c-, cleaved.