Since peroxisome proliferator-activated receptor gamma (PPARgamma) acts as a regulator of CNS inflammation and a powerful pharmacological target for counteracting CNS diseases, we investigated the role of the PPARgamma agonist, rosiglitazone, in the modulation of CD40 expression and in the pathological processes of inflammation after SE.
Based on these results, we propose that PPAR-gamma gene has the inherent capacity to influence the lipid mediated inflammation process in atherosclerotic lesions.