Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4348821 | Neuroscience Letters | 2008 | 4 Pages |
Abstract
We created an inflammation-induced Parkinson's disease model, where microglia activation leads to oxidative stress, mitochondrial dysfunction, and dopaminergic neurodegeneration in the substantia nigra. Pioglitazone, an agonist of peroxisome proliferator activated receptor-gamma (PPAR-γ), can prevent these deficits and protect dopaminergic neurons. To continue exploring the effects of pioglitazone in this model we focused on the expression of PPAR-γ, uncoupling protein 2 (UCP2), and mitoNEET. We report that intrastriatal lipopolysaccharide (LPS) increases striatal PPAR-γ, UCP2, and mitoNEET expression, and pioglitazone attenuates these LPS-induced changes.
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Authors
Randy L. Hunter, Dong-Young Choi, Stuart A. Ross, Guoying Bing,