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dc.contributor.authorRen Tong
dc.contributor.authorLiu Jinfeng
dc.contributor.authorGe Yunlong
dc.contributor.authorZhuo Rengong
dc.contributor.authorPeng Lu
dc.contributor.authorLiu Feng
dc.contributor.authorJin Xin
dc.contributor.authorYang Lichao
dc.date.accessioned2020-10-10T02:09:27Z
dc.date.available2020-10-10T02:09:27Z
dc.date.issued2019-10-06
dc.identifier.citationNeurochemistry international,2019,
dc.identifier.other10.1016/j.neuint.2019.104501
dc.identifier.urihttps://dspace.xmu.edu.cn/handle/2288/174882
dc.description.abstractBrain is a site of diabetic end-organ damage. Diabetes-associated cognitive dysfunction, referred as "diabetic encephalopathy" (DE) has been coined for the patients with type 2 diabetes mellitus showing decline in their cognitive function, especially weak episodic memory, cognitive inflexibility and poor psychomotor performance leading towards Alzheimer’s disease. Current evidence supported that aberrant synapses, energy metabolism imbalance, advanced glycation end products (AGEs) accumulation and Tau hyperphosphorylation are associated with cognition deficits induced by diabetes. Oleoylethanolamide (OEA), an endogenous peroxisome proliferator-activated receptor alpha (PPARα) agonist, has anti-hyperlipidemia, anti-inflammatory and neuroprotective activities. However, the effect of OEA on DE is unknown. Therefore, we tested its influence against cognitive dysfunction in high fat diet and streptozotocin (HFD + STZ)-induced diabetic C57BL/6J and PPARα--/- mice using Morris water maze (MWM) test. Neuron staining, dementia markers and neuroplasticity in the hippocampus were assessed to evaluate the neuropathological changes. The results showed that chronic OEA treatment significantly lowered hyperglycemia, recovered cognitive performance, reduced dementia markers, and inhibited hippocampal neuron loss and neuroplasticity impairments in diabetic mice. In contrast, the changes in MWM performance and neuron loss were not observed in PPARα knockout mice via OEA administration. These results indicated that OEA may provide a potential alternative therapeutic for DE by activating PPARα signaling.
dc.language.isozh_CN
dc.subjectDiabetic encephalopathy
dc.subjectNeuroprotection
dc.subjectOleoylethanolamide
dc.subjectPeroxisome proliferator-activated receptor alpha
dc.subjectSpatial cognitive function
dc.titleChronic oleoylethanolamide treatment attenuates diabetes-induced mice encephalopathy by triggering peroxisome proliferator-activated receptor alpha in the hippocampus.
dc.typeArticle


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