PPAR-γ agonist rosiglitazone decreases focal cerebral ischemia-induced inflammation and brain damage in adult mice
| Autor: | Ramya Sundaresan, Kellie K. Bowen, Raghu Vemuganti, Kudret Türeyen |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
chemistry.chemical_classification
medicine.medical_specialty Ischemia Peroxisome proliferator-activated receptor Inflammation Brain damage Biology medicine.disease PPAR agonist Endocrinology Neurology chemistry Internal medicine medicine Neurology (clinical) medicine.symptom Cardiology and Cardiovascular Medicine Receptor Rosiglitazone Pioglitazone medicine.drug |
| Zdroj: | Journal of Cerebral Blood Flow & Metabolism. 25:S94-S94 |
| ISSN: | 1559-7016 0271-678X |
| DOI: | 10.1038/sj.jcbfm.9591524.0094 |
| Popis: | Acute inflammation contributes to brain damage after focal cerebral ischemia. Although several transcription factors are known to be upregulated in the post-ischemic brain, the role of transcriptional events in controlling cerebral inflammation is not evaluated in detail. Peroxisome proliferation activated receptor- (PPAR-) is a ligand activated transcription factor of nuclear hormone receptor superfamily. When a ligand binds to PPAR-, it dimerizes with retinoic acid-X-receptor (RXR) to form a heterodimeric complex that binds to the cis-acting sequences (peroxisome proliferator response elements) on DNA to modulate the transcription of target genes. Thiozolinediones rosiglitazone and pioglitazone are potent exogenous agonists of PPAR-. Rosiglitazone and pioglitazone are currently FDA-approved for the treatment of type-2 diabetes. PPAR- agonists were shown to control inflammation associated with gut, myocardial and lung ischemia by blocking microglia/macrophage activation and pro-inflammatory gene expression. We evaluated the efficacy of rosiglitazone in preventing brain damage following transient middle cerebral artery occlusion (MCAO) in adult C57/BL6 mice. Real-time PCR analysis showed significant increases (by 2.7 to 4.2 fold; p |
| Databáze: | OpenAIRE |
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