Role of PPAR<img src='/image/spc_char/gamma2.gif' border=0>, a Nuclear Hormone Receptor in Neuroprotection

Abstract

Peroxisome proliferator-activated receptors (PPARs) belong to the nuclear receptor superfamily. PPAR-alpha is involved in wound healing, stimulation of lipid and folic acid catabolism, inflammation control, inhibition of ureagenesis and peroxisome proliferation. The PPAR<img src='/image/spc_char/beta.gif' border=0>/<img src='/image/spc_char/delta1.gif' border=0> is involved wound healing, cell proliferation, embryo implantation, adipocyte differentiation, myelination alteration and apoptosis. The PPAR<img src='/image/spc_char/gamma2.gif' border=0> is involved in fat, lipid and calorie utilization, sugar control, inflammation control and macrophage (MQ) matutation. Homocysteine (Hcy) binds to nuclear peroxisome proliferator activated receptor. Increase in PPAR expression decreases the level of nitrotyrosine and increases endothelial nitric oxide concentration, decreases metalloproteinase activity and expression as well as elastinolysis and reverses Hcy-mediated vascular dysfunction. The PPAR<img src='/image/spc_char/gamma2.gif' border=0> initially recognized as a regulator of adipocyte development has become a potential therapeutic target for the treatment of diverse disorders. In addition, the activation of PPAR<img src='/image/spc_char/gamma2.gif' border=0> receptor ameliorates neurodegenerative disease. This review focuses on the recent knowledge of PPAR<img src='/image/spc_char/gamma2.gif' border=0> in neuroprotection and deals with the mechanism of neuroprotection of central nervous system disorder by PPAR<img src='/image/spc_char/gamma2.gif' border=0>.