Strokes are often caused by a blockage of blood flow in the brain, referred to as ischemia, which results in a shortage of oxygen to the brain. Vascular degradation after cerebral ischemia leads to BBB disruption and neuronal loss. Of the three PPAR isotypes, PPARδ is the highest expressed in the brain's parenchyma and cerebral vasculature, and increasing evidence suggests that PPARδ may protect against ischemic insults [13]. This was first highlighted in PPARδ-null mice, which compared to WT mice, had a significant increase in infarct size after focal cerebral ischemia [17, 18]. The difference in infarct size was detected as early as 30 min after induction of ischemia, suggesting that PPARδ plays an early role in protection [17]. Following middle cerebral artery occlusion (MCAO), increased cerebrovascular permeability and infarct size were detected in mice with specific deletion of PPARδ in vascular smooth muscle cells (VSMCs) [13]. Additionally, PPARδ agonists appear to be protective after cerebral ischemia; rats given infusions of L-165041 or GW501516 had significantly attenuated ischemic damage 24 h after MCAO [12]. The mechanisms underlying the protective effect
