The modulatory mechanisms of fenofibrate on human primary T cells

Abstract

Fenofibrate is a lipid-lowering agent and supposed to have anti-inflammatory properties. But it was rarely evaluated for the signal transduction on human primary T cells. Therefore, the methods including enzyme-linked immunosorbent assay (ELISA), electrophoretic mobility shift assay, luciferase assay and Western blotting were used to investigate the mechanisms of fenofibrate on human primary T cells, isolated from normal human beings. We found that fenofibrate could dose-dependently inhibit cytokine production such as interleukin-2, interleukin-4, tumor necrosis factor-alpha and interferon-gamma from activated T cells. Also, it could down-regulate activator protein-1 (AP-1) DNA-binding activities in T cells. As performing in vivo study, fenofibrate reduced the AP-1 transcriptional activity in Jurkat cells. Finally, fenofibrate inhibited the activation of c-Jun NH 2-terminal protein kinase and P38 mitogen-activated protein kinase. These results may extend potential therapeutic mechanisms of fenofibrate on cardiovascular disease with inflammatory processes.