Gillespie William, Tyagi Neetu, Tyagi Suresh C
Department of Physiology & Biophysics, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA.
Indian J Biochem Biophys. 2011 Apr;48(2):73-81.
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 PPARgamma/delta is involved wound healing, cell proliferation, embryo implantation, adipocyte differentiation, myelination alteration and apoptosis. The PPARgamma 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 PPARgamma 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 PPARgamma receptor ameliorates neurodegenerative disease. This review focuses on the recent knowledge of PPARgamma in neuroprotection and deals with the mechanism of neuroprotection of central nervous system disorder by PPARgamma.
过氧化物酶体增殖物激活受体（PPARs）属于核受体超家族。PPAR-α参与伤口愈合、刺激脂质和叶酸分解代谢、控制炎症、抑制尿素生成以及过氧化物酶体增殖。PPARγ/δ参与伤口愈合、细胞增殖、胚胎着床、脂肪细胞分化、髓鞘形成改变和细胞凋亡。PPARγ参与脂肪、脂质和热量利用、血糖控制、炎症控制以及巨噬细胞（MQ）突变。同型半胱氨酸（Hcy）与核过氧化物酶体增殖物激活受体结合。PPAR表达增加会降低硝基酪氨酸水平并增加内皮一氧化氮浓度，降低金属蛋白酶活性和表达以及弹性蛋白溶解，并逆转Hcy介导的血管功能障碍。PPARγ最初被认为是脂肪细胞发育的调节因子，现已成为治疗多种疾病的潜在治疗靶点。此外，PPARγ受体的激活可改善神经退行性疾病。本综述聚焦于PPARγ在神经保护方面的最新知识，并探讨PPARγ对中枢神经系统疾病的神经保护机制。
