Role of PPAR<img src='/image/spc_char/gamma2.gif' border=0>, a Nuclear Hormone Receptor in Neuroprotection
NOPR - NISCAIR Online Periodicals Repository
View Archive InfoField | Value | |
Title |
Role of PPAR, a Nuclear Hormone Receptor in Neuroprotection
|
|
Creator |
Gillespie, William
Tyagi, Neetu Tyagi, Suresh C |
|
Subject |
PPAR
Neuronal death Ischemia Neurodegenerative disorder Alzheimer’s disease Parkinson’s disease Multiple Sclerosis |
|
Description |
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 PPAR/ is involved wound healing, cell proliferation, embryo implantation, adipocyte differentiation, myelination alteration and apoptosis. The PPAR 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 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 receptor ameliorates neurodegenerative disease. This review focuses on the recent knowledge of PPAR in neuroprotection and deals with the mechanism of neuroprotection of central nervous system disorder by PPAR. |
|
Date |
2011-04-26T06:51:01Z
2011-04-26T06:51:01Z 2011-04 |
|
Type |
Article
|
|
Identifier |
0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/11608 |
|
Language |
en_US
|
|
Rights |
CC Attribution-Noncommercial-No Derivative Works 2.5 India
|
|
Publisher |
NISCAIR-CSIR, India
|
|
Source |
IJBB Vol.48(2) [April 2011]
|
|