The effect of activation of peroxisome proliferator-activated receptor gamma (PPARγ) on human monocyte function:: PPARγ ligands do not inhibit tumor necrosis factor-α release in human monocytic cell line THP-1

Peroxisome proliferator-activated receptor gamma (PPAR gamma) activation by its ligands reportedly inhibits monocyte function. However, because the concentrations of PPAR gamma ligands used in previous studies were higher than typically expected to activate PPAR gamma, we clarified whether PPAR gamma ligands influence monocyte function and cell viability of the human monocyte cell line THP-1. We determined tumor necrosis factor-alpha (TNF-alpha) release as a monocyte function and cell viability using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide. Both troglitazone and 15-deoxy-Delta(12,14)-prostaglandin J(2) (15-d-PGJ2) seemed to inhibit phorbol ester-induced TNF-alpha release from THP-1 cells. On the other hand, neither pioglitazone nor rosiglitazone inhibited phorbol ester-induced TNF-alpha release. Because the cytotoxicity of troglitazone and 15-d-PGJ2 was significantly (p < 0.05, Tukey-Kramer) stronger than that of pioglitazone and rosiglitazone, the inhibition of TNF-alpha release seemed to parallel the lack of cell viability. We concluded that PPAR gamma ligands did not directly inhibit TNF-alpha release in THP-1 cells.