Amelioration of experimental autoimmune encephalomyelitis in C57BL/6 mice by an agonist of peroxisome proliferator-activated receptor-gamma.
Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a member of the nuclear hormone receptor superfamily, plays a critical role in adipocyte differentiation and glucose homeostasis. It has been implicated that PPAR-gamma functions as a regulator of cellular proliferation and inflammatory responses. In the present study, we examined whether troglitazone, a selective PPAR-gamma agonists, ameliorated experimental autoimmune encephalomyelitis (EAE) induced by administration of myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 in C57BL/6 mice. We found that troglitazone attenuated the inflammation and decreased the clinical symptoms. It was suggested that the amelioration was attributed to the attenuation of pro-inflammatory cytokine gene expressions.
Item Type | Article |
---|---|
Keywords | Animal, Cell Division, drug effects, Chromans, pharmacology, Cytokines, genetics, Encephalomyelitis, Experimental Autoimmune, immunology, pathology, prevention & control, Female, Inflammation Mediators, physiology, Mice, Mice, Inbred C57BL, Myelin-Associated Glycoprotein, immunology, Peptide Fragments, immunology, RNA, Messenger, antagonists & inhibitors, Receptors, Cytoplasmic and Nuclear, agonists, Reference Values, Support, Non-U.S. Gov't, T-Lymphocytes, pathology, Thiazoles, pharmacology, Transcription Factors, agonists |
ISI | 168204100006 |