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. Author manuscript; available in PMC: 2010 Jan 1.
Published in final edited form as: Immunopharmacol Immunotoxicol. 2009;31(3):339–351. doi: 10.1080/08923970902785253

Figure 3. PPAR-α-independent action of gemfibrozil.

Figure 3

Anti-inflammatory, anti-oxidative and immuno-modulatory activities of gemfibrozil do not depend on PPAR-α. In one mechanism, gemfibrozil binds and stimulates the recruitment of human S μ binding protein-2 (HSµBP-2), glial factor-1 (GF-1), and possibly aryl hydrocarbon receptor (Ahr) at the drug responsive element (DRE) of numerous anti-inflammatory as well as neurotrophic genes. In another pathway, gemfibrozil is able to stimulate phosphatidylinositol-3 (PI-3) kinase via an unknown PPAR-α-independent mechanism. Once PI-3 kinase is activated, it stimulates the expression of inhibitory kappa B-alpha (IκBα) molecule, which in turn binds with functionally active NF-κB molecule and arrests the nuclear migration of NF-κB complex.