Abstract
Increasing evidence links neuroinflammation to Parkinson's disease. Microglia are mediators of neuroinflammation. Overactivation of microglia contributes to the release of cyclooxygenase 2 and prostaglandin E2 during neuronal insults. We have previously shown that pioglitazone, a peroxisome proliferator-activated receptor gamma agonist, inhibits microglia activation, reduces proinflammatory factors, and protects dopaminergic neurons. Here, we demonstrated that pioglitazone protects dopaminergic neurons by inhibiting abnormal microglia activation, interfering with phosphorylation of jun N-terminal kinase and nuclear factor kappa-B, and by suppressing cyclooxygenase 2 expression and the subsequent prostaglandin E2 synthesis. Therefore, the anti-inflammatory properties of pioglitazone may be useful for ameliorating the progression of Parkinson's disease.
Original language | English |
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Pages (from-to) | 89-98 |
Number of pages | 10 |
Journal | Journal of Neuroimmunology |
Volume | 192 |
Issue number | 1-2 |
DOIs | |
State | Published - Dec 2007 |
Bibliographical note
Funding Information:The authors wish to thank Randy Hunter for his help in writing and Mei Liu for her double-immunostaining technique. The present work was supported by NIH grant NS044157 (GB).
Keywords
- COX-2
- Dopaminergic neurons
- JNK
- Microglia
- NF-κB
- PGE
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology