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P82 Inflammation plays a critical role in the generation of  ischemic injury. Ischemic insult results in the activation of microglia  and secretion of proinflammatory products including the cytokines  interleukin-1β and tumor necrosis factor-α. Both of these cytokines  exacerbate ischemic injury. Microglial proinflammatory gene expression  is regulated by the transcription factor peroxisome proliferator  activated receptor (PPAR). PPARγ is a member of the nuclear hormone  receptor family and upon binding of agonist acts to inhibit  proinflammatory gene expression. We hypothesized that PPARγ agonists  reduce the inflammatory reaction seen following stroke and limit  infarction size. We utilized a reversible model of middle cerebral  artery occlusion to induce two hours of ischemia in rats to test our  hypothesis. Blood pressure, blood gases and temperature were monitored  and maintained within normal ranges throughout the procedure. Vehicle  (DMSO) or troglitazone, a PPARγ agonist previously approved by the  FDA, was administered to rats twenty-four hours before and again at the  time of occlusion in doses of 35, 70 or 100 mg/kg in DMSO. Twenty-four  hours after occlusion animals were euthanized. Infarct volume was  calculated from fixed frozen sections and additional sections were  processed for immunocytochemistry. Results show over sixty percent  reduction in infarct volume in rats treated with 35 mg/kg and 70 mg/kg  troglitazone. These data were statistically significant (n≥5;p&lt;0.05).  Interestingly the 100 mg/kg dose of troglitazone did not protect  against ischemia. Immunoreactivity against the proinflammatory  cytokines Il-1β and TNFα was reduced in the peri-infarct region of  troglitazone treated rats. Furthermore, immunoreactivity against other  markers of inflammation, intracellular adhesion molecule, major  histocompatibility complex antigen I and cyclooxygenase-2 was also  reduced in troglitazone treated animals compared with vehicle treated  animals. These data indicate that the PPARγ agonist, troglitazone,  reduces infarct size following cerebral ischemia likely due to the  drug’s anti-inflammatory properties.

A PPARγ agonist reduces proinflammatory cytokine immunoreactivity and infarct size following transient focal ischemia in rats