Isoflavones and PPAR Signaling: A Critical Target in Cardiovascular, Metastatic, and Metabolic Disease
Figure 4
Isoflavones inhibit TNFα-induced monocyte adhesion to the vascular wall via activation of PPARγ. Both genistein (1 μM) and rosiglitazone (2 μM) significantly reduced TNFα-induced monocyte adhesion to the vascular wall compared to TNFα alone. This inhibition was reversed by the PPARγ antagonist, GW 9662 (5 μM), revealing that genistein’s inhibitory effect was PPARγ dependent (reproduced with permission by the American Journal of Physiology).
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