作者：REN; Tong; LIU; Jin-feng; ZHUO; Ren-go...oleoylethanolamidespatialcognitivefunctionneuroprotectionperoxisomereceptoralpha
摘要：OBJECTIVE Oleoylethanolamide (OEA) is an endogenous peroxisome proliferatoractivated receptor alpha (PPARα) agonist that acts on the peripheral control of energy metabolism. Previous studies have shown that OEA exerts neuroprotection after cerebral ischemia. However, whether OEA affects the outcomes of diabetes-induced encephalopathy (DE) requires further study. METHODS The chronic effects of OEA on DE were evaluated in C57BL / 6 and PPARα knockout mice, individually. The cognitive function was assessed with Morris water maze. The expression of receptor for advanced glycation end products (RAGE) and phosphorylation of Tau in mice hippocampus were determined using Western blotting. The influence of OEA in neuron loss and neuroplasticity were assessed with immunofluorescent staining and Western blotting. RESULTS OEA markedly ameliorated performance in the Morris water maze, which was correlated with its capabilities of suppressing glycometabolism and phosphorylation of Tau in the hippocampus. OEA offered protection from diabetes-induced impairments in hippocampal neu-roplasticity. Furthermore, the changes in Morris water maze performance and neuron loss could not be observed in PPARα knockout mouse models with OEA administration. CONCLUSION The ability of OEA to control PPARα signaling can serve as a novel neuroprotective approach for the treatment of diabetes-induced encepha-lopathy.
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