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Molecules 2016, 21(8), 1093; doi:10.3390/molecules21081093

Neuroprotection by Combined Administration with Maslinic Acid, a Natural Product from Olea europaea, and MK-801 in the Cerebral Ischemia Model

1
Institute of Translational Medicine, Nanchang University, 1299 Xuefu Avenue, Nanchang 330001, China
2
Department of Physiology, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China
3
Department of Human Anatomy and Cell Science, University of Manitoba, 745 Bannatyne Avenue, Winnipeg, MB R3E 0J9, Canada
4
Center for Drug Discovery, China Pharmaceutical University, 24 Tongjiaxiang Street, Nanjing 210009, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Peter Koulen
Received: 19 June 2016 / Revised: 15 August 2016 / Accepted: 17 August 2016 / Published: 19 August 2016
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Abstract

Glutamate-mediated excitotoxicity is a major cause of ischemic brain damage. MK-801 confers neuroprotection by attenuating the activation of the N-methyl-d-aspartate (NMDA) receptor, but it failed in clinical use due to the short therapeutic window. Here we aim to investigate the effects of maslinic acid, a natural product from Olea europaea, on the therapeutic time window and dose range for the neuroprotection of MK-801. Rats were administered with maslinic acid intracerebroventricularly and cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) followed by reperfusion. MK-801 was administered at 1 h, 2 h, 3 h and 4 h after ischemia, respectively. The cerebral infarct volume was determined by 2,3,5-Triphenyltetrazolium chloride (TTC) staining, neuronal damage was assessed by Haematoxylin Eosin (H&E) staining, and the expression of glial glutamate transporters and glial fibrillary acidic protein (GFAP) was evaluated by immunohistochemistry and Western blot post-ischemia. Results showed that the presence of maslinic acid extended the therapeutic time window for MK-801 from 1 h to 3 h. Co-treatment of maslinic acid and MK-801 at a subthreshold dosage obviously induced neuroprotection after ischemia. The combination of these two compounds improved the outcome in ischemic rats. Moreover, maslinic acid treatment promoted the expression of GLT-1 and GFAP post-ischemia. These data suggest that the synergistic effect of maslinic acid on neurological protection might be associated with the improvement of glial function, especially with the increased expression of GLT-1. The combination therapy of maslinic acid and MK-801 may prove to be a potential strategy for treating acute ischemic stroke. View Full-Text
Keywords: cerebral ischemia; maslinic acid; MK-801; GLT-1 cerebral ischemia; maslinic acid; MK-801; GLT-1
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Qian, Y.; Tang, X.; Guan, T.; Li, Y.; Sun, H. Neuroprotection by Combined Administration with Maslinic Acid, a Natural Product from Olea europaea, and MK-801 in the Cerebral Ischemia Model. Molecules 2016, 21, 1093.

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