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Title: | Regulation of inflammatory response in neural cells in vitro by thiadiazolidinones derivatives through peroxisome proliferator-activated receptor γ activation |
Authors: | Luna Medina, Rosario de ![]() ![]() ![]() ![]() |
Issue Date: | 2005 |
Publisher: | American Society for Biochemistry and Molecular Biology |
Citation: | Journal of Biological Chemistry 280(22): 21453-21462 (2005) |
Abstract: | In 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 |
URI: | http://hdl.handle.net/10261/81208 |
DOI: | 10.1074/jbc.M414390200 |
Identifiers: | doi: 10.1074/jbc.M414390200 issn: 0021-9258 e-issn: 1083-351X |
Appears in Collections: | (IIBM) Artículos |
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