| Literature DB >> 25748831 |
Li-Chao Yang1, Han Guo1, Hao Zhou1, Da-Qin Suo1, Wen-Jun Li1, Yu Zhou1, Yun Zhao1, Wu-Shuang Yang2, Xin Jin3.
Abstract
Oleoylethanolamide (OEA) has been shown to have neuroprotective effects after acute cerebral ischemic injury. The aim of this study was to investigate the effects of chronic OEA treatment on ischemia-induced spatial cognitive impairments, electrophysiology behavior and hippocampal neurogenesis. Daily treatments of 30 mg/kg OEA significantly ameliorated spatial cognitive deficits and attenuated the inhibition of long-term potentiation (LTP) in the middle cerebral artery occlusion (MCAO) rat model. Moreover, OEA administration improved cognitive function in a manner associated with enhanced neurogenesis in the hippocampus. Further study demonstrated that treatment with OEA markedly increased the expressions of brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptors α (PPARα). Our data suggest that chronic OEA treatment can exert functional recovery of cognitive impairments and neuroprotective effects against cerebral ischemic insult in rats via triggering of neurogenesis in the hippocampus, which supports the therapeutic use of OEA for cerebral ischemia.Entities:
Keywords: 3-Aminobenzamide (PubChem CID: 1645); 3′-Azido-deoxythymidine (PubChem CID: 451515); 5-Bromo-2′-deoxyuridine (PubChem CID: 6035); Focal cerebral ischemia; Hippocampal neurogenesis; Oleoylethanolamide; Oleoylethanolamide (PubChem CID: 5283454); Rats; Spatial cognitive function
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Year: 2015 PMID： 25748831 DOI： 10.1016/j.bcp.2015.02.012
Source DB: PubMed Journal: Biochem Pharmacol ISSN： 0006-2952 Impact factor: 5.858