The present study was designed to investigate the pattern of time-dependent expression of peroxisome proliferator-activated receptors (PPARα, β, and γ) after global cerebral ischemia and reperfusion (I/R) damage in the rat hippocampus. Male Sprague Dawley (SD) rats were subjected to global cerebral I/R. The rat hippocampi were isolated to detect the expression of PPARs mRNA and protein levels at 30？min–30？d after I/R by RT-PCR and Western blot analysis, respectively. The expression levels of PPARs mRNA and protein in the rat hippocampus significantly increased and peaked at 24？h for PPARα and γ (at 48？h for PPARβ) after I/R, then gradually decreased, and finally approached control levels on d？30. The present results suggest that global cerebral I/R can cause obvious increases of hippocampal PPARs mRNA and protein expression within 15？d after I/R. These findings may help to guide the experimental and clinical therapeutic use of PPARs agonists against brain injury. 1. Introduction Cerebral ischemic injury is the second leading cause of death and a common cause of disability worldwide. Cerebral ischemia can be divided into two groups: global cerebral ischemia and focal cerebral ischemia. The major manifestation of cerebral ischemia is a temporal or permanent reduction in cerebral blood flow, which is insufficient to meet the metabolic or functional demand of the central nervous system (CNS). There was no reperfusion after permanent occlusion of artery. Following transient ischemia or treatment of thrombolysis, reperfusion inevitably occurs. Although the reperfusion is helpful for restoring the supply of blood and oxygen to the CNS, a growing body of evidence supports the viewpoint that reperfusion may exacerbate the injury initially resulting from ischemia and is referred to as cerebral ischemia and reperfusion (I/R) injury. Cerebral I/R can cause serious neuronal injury and death, which can further lead to learning and memory impairment and neurodegeneration. The pyramidal neurons of the hippocampal CA1 region are essential for spatial learning and memory functions. When suffering from cerebral ischemia insult, the hippocampal pyramidal neurons are the most vulnerable to the reduction of blood supply to the brain, and cell death occurs days after the initial ischemic insult, a phenomenon termed “delayed neuronal death” [1]. Currently, the mechanisms of neuronal injury and death induced by cerebral I/R are not completely known, and therefore an effective therapy for ischemic cerebral damage has remained elusive. Recently, much evidence has emerged
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