Figure 6

PPARγ inhibits atherosclerotic plaque formation by suppressing TLR4-mediated inflammation and ACAT1 expression. (a–c) HF diet significantly induced TLR4, proinflammatory cytokines and ACAT1 expressions in ApoE^−/− mice, which were significantly abrogated by the PPARγ agonist, RSG. In contrast, ApoE/TLR4^−/− mice displayed an undetectable effect on proinflammatory cytokines and ACAT1 in response to RSG. (d) HF diet significantly inhibited the level of PPARγ in ApoE^−/− mice, which were reversed by RSG. TLR4 deficiency exerted undetectable influence on the expression of PPARγ in vivo (*P<0.05 versus ApoE^−/− mice with NC diet; ^#P<0.05 versus ApoE^−/− mice with HF diet). Results were presented as mean±S.D. (error bars) of three independent experiments