English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/81208
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE
Exportar a otros formatos:


Regulation of inflammatory response in neural cells in vitro by thiadiazolidinones derivatives through peroxisome proliferator-activated receptor γ activation

AuthorsLuna Medina, Rosario de ; Cortés-Canteli, Marta ; Alonso Cascón, Mercedes; Santos, Ángel; Martínez, Ana ; Pérez Castillo, Ana
Issue Date2005
PublisherAmerican Society for Biochemistry and Molecular Biology
CitationJournal of Biological Chemistry 280(22): 21453-21462 (2005)
AbstractIn most neurodegenerative disorders, including multiple sclerosis, Parkinson disease, and Alzheimer disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated astrocytes and microglia and their cytotoxic agents play a crucial pathological role. Current treatments for these diseases are not effective. In the present study we investigate the effect of thiadiazolidinone derivatives, which have been recently suggested to play a role in neurodegenerative disorders. We have found that thiadiazolidinones are potent neuroprotector compounds. Thiadiazolidinones inhibited inflammatory activation of cultured brain astrocytes and microglia by diminishing lipopolysaccharide-induced interleukin 6, tumor necrosis factor a, inducible nitric-oxide synthase, and inducible cyclooxygenase type 2 expression. In addition, thiadiazolidinones inhibited tumor necrosis factor-α and nitric oxide production and, concomitantly, protected cortical neurons from cell death induced by the cell-free supernatant from activated microglia. The neuroprotective effects of thiadiazolidinones are completely inhibited by the peroxisome proliferator-activated receptor γ antagonist GW9662. In contrast the glycogen synthase kinase 3β inhibitor LiC1 did not show any effect. These findings suggest that thiadiazolidinones potently attenuate lipopolysaccharide-induced neuroinflammation and reduces neuronal death by a mechanism dependent of peroxisome proliferator-activated receptor γ activation. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
Publisher version (URL)http://dx.doi.org/10.1074/jbc.M414390200
Identifiersdoi: 10.1074/jbc.M414390200
issn: 0021-9258
e-issn: 1083-351X
Appears in Collections:(IIBM) Artículos
Files in This Item:
File Description SizeFormat 
peroxisome proliferator-activated.pdf2,95 MBAdobe PDFThumbnail
Show full item record
Review this work

Related articles:

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.