In terms of preclinical use of OEA in acute ischemic stroke treatment, an experimental study on Sprague Dawley rats demonstrated that chronic OEA therapy (30 mg/kg/day for 28 days) can promote neurogenesis in the hippocampus through increasing the expression of brain-derived neurotrophic factor (BDNF) and PPAR-α resulting in functional recovery of cognitive deficits and neuroprotective benefits against cerebral ischemic insult, indicating that OEA might be used therapeutically for cerebral ischemia [48]. This evidence concerns the gene PPARA and Cerebral ischemia.