Protective properties afforded by pioglitazone against intrastriatal LPS in Sprague-Dawley rats - PubMed (original) (raw)
Protective properties afforded by pioglitazone against intrastriatal LPS in Sprague-Dawley rats
Randy L Hunter et al. Neurosci Lett. 2008.
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-gamma), 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-gamma, uncoupling protein 2 (UCP2), and mitoNEET. We report that intrastriatal lipopolysaccharide (LPS) increases striatal PPAR-gamma, UCP2, and mitoNEET expression, and pioglitazone attenuates these LPS-induced changes.
Figures
Figure 1
Western blot analysis shows a trend for LPS to increase PPAR-γ expression. In addition, LPS significantly increases both UCP2 and mitoNEET. Treatment with pioglitazone significantly attenuates the LPS-induced increase in PPAR-γ, UCP2, and mitoNEET (Figure 1A). Data are expressed as means +/−SEM, from n=3–5/group, ** or ## = p≤ 0.01, where ** represents Vehicle/Saline (V/S) vs. Vehicle/LPS (V/L) and ## represents Vehicle/LPS vs. Pioglitazone/LPS (P/L). Figure 1B shows representative blots for PPAR-γ, UCP2, mitoNEET, and beta-actin.
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