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15-Deoxy-Δ 12,14 -prostaglandin J 2  (15d-PGJ 2 ) and activin are implicated in the control of apoptosis, cell proliferation, and inflammation in cells. We examined both the mechanism by which 15d-PGJ 2  regulates the transcription of activin-induced activin receptors (ActR) and Smads in HepG2 cells and the involvement of the nuclear factor-  κ  B (NF-  κ  B) and mitogen-activated protein kinase (MAPK) pathways in this regulation. Activin A (25 ng/mL) inhibited HepG2 cell proliferation, whereas 15d-PGJ 2  (2   μ  M and 5   μ  M) had no effect. Activin A and 15d-PGJ 2  showed different regulatory effects on ActR and Smad expression, NF-  κ  B p65 activity and MEK/ERK phosphorylation, whereas they both decreased IL-6 production and increased IL-8 production. When co-stimulated with 15d-PGJ 2  and activin, 15d-PGJ 2  inhibited the activin-induced increases in ActR and Smad expression, and decreased activin-induced IL-6 production. However, it increased activin-induced IL-8 production. In addition, 15d-PGJ 2  inhibited activin-induced NF-  κ  B p65 activity and activin-induced MEK/ERK phosphorylation. These results suggest that 15d-PGJ 2  suppresses activin-induced ActR and Smad expression, down-regulates IL-6 production, and up-regulates IL-8 production via suppression of NF-  κ  B and MAPK signaling pathway in HepG2 cells. Regulation of ActR and Smad transcript expression and cytokine production involves NF-  κ  B and the MAPK pathway via interaction with 15d-PGJ 2 /activin/Smad signaling.

ppar research

15-deoxy-Δ12,14-prostaglandin J2Down-Regulates Activin-Induced Activin Receptor, Smad, and Cytokines Expression via Suppression of NF-κB and MAPK Signaling in HepG2 Cells