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\nactivities exerted through a variety of different mechanisms. Some curcumin effects have been reported to involve
\nactivation of the nuclear transcription factor peroxisome proliferator-activated receptor-? (PPAR-?), but the
\nconcept that curcumin might be a PPAR-? ligand remains controversial. Results reported here demonstrate that, in
\ncontrast to the PPAR-? ligands ciglitazone and rosiglitazone, curcumin is inactive in five different reporter or DNA-
\nbinding assays, does not displace [3H]rosiglitazone from the PPAR-? ligand-binding site, and does not induce
\nPPAR-?-dependent differentiation of preadipocytes, while its ability to inhibit fibroblast-to-myofibroblast
\ndifferentiation is not affected by any of four PPAR-? antagonists. These multiple lines of evidence conclusively
\ndemonstrate that curcumin is not a PPAR-? ligand and indicate the need for further investigation of the
\nmechanisms through which the compound acts.
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