The Macrophage-Mediated Effects of the Peroxisome Proliferator-Activated Receptor-Gamma Agonist Rosiglitazone Attenuate Tactile Allodynia in the Early Phase of Neuropathic Pain Development

Rosiglitazone Allodynia
DOI: 10.1213/ane.0b013e31821b220c Publication Date: 2011-04-14T07:41:52Z
ABSTRACT
In Brief BACKGROUND: Neuroinflammation triggered by macrophage infiltration into sites of peripheral nerve injury may result in neuropathic pain. Peroxisome proliferator-activated receptor (PPAR)γ signaling regulates the properties macrophages. However, macrophage-mediated effects PPARγ on pain inflammation have not been investigated. METHODS: To evaluate tactile allodynia, we administered blood-brain barrier–impermeant agonist, rosiglitazone, after partial sciatic ligation (PSNL) as (1) systemic treatment during different phases development, (2) local injection to PSNL site early phase, or (3) peritoneal macrophages pretreated with rosiglitazone transplanted site. addition, direct effect was evaluated activated interferon-γ. RESULTS: Systemic course progressive ameliorated infiltration, and production proinflammatory mediators including cyclooxygenase-2, inducible nitric oxide synthase, matrix metalloprotease 9 at Local transplantation rosiglitazone-treated significantly improved allodynia. macrophages, down-regulated interferon-γ–induced gene expression cyclooxygenase-2 synthase attenuated chemotactic response monocyte protein-1. DISCUSSION: Rosiglitazone phase alleviated development allodynia regulating molecules inflamed Our results indicate that activation suppress development. Published ahead print April 13, 2011
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