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, 89 (11), 1829-39

Maslinic Acid, a Natural Inhibitor of Glycogen Phosphorylase, Reduces Cerebral Ischemic Injury in Hyperglycemic Rats by GLT-1 Up-Regulation

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Maslinic Acid, a Natural Inhibitor of Glycogen Phosphorylase, Reduces Cerebral Ischemic Injury in Hyperglycemic Rats by GLT-1 Up-Regulation

Teng Guan et al. J Neurosci Res.

Abstract

Maslinic acid (MA), a natural triterpene from Olea europaea L., is a well-known inhibitor of glycogen phosphorylase and elicits multiple biological activities. The purpose of this study was to evaluate the effects of MA on focal cerebral ischemia in hyperglycemic rats. Adult rats were made hyperglycemic by intraperitoneal injection of streptozotocin and were given MA (50 mg/kg or 5 mg/kg) intragastrically for 14 consecutive days. Transient middle cerebral artery occlusion/reperfusion was then induced by a suture insertion technique. Results showed that diabetic rats pretreated with high-dose MA had lower blood glucose levels, but both doses reduced infarct volumes and improved neurological scores. Less glutamate overflow was also observed in MA-treated rats after 2 hr of ischemia followed by 24 hr and 72 hr reperfusion. In addition, MA treatment enhanced the glial glutamate transporter GLT-1 expression at the protein and mRNA levels. However, the injection of dihydrokainate, a GLT-1 glutamate transporter inhibitor, reversed the effect of MA. Previous studies have shown that suppression of glutamate uptake via nuclear factor-κB (NF-κB) activation is an important contributory factor in ischemia-triggered glutamate excitotoxicity, and inhibition of NF-κB could prevent ischemic suppression of glutamate uptake and GLT-1 expression. In the present study, we showed that MA pretreatment attenuated ischemia-induced translocation of NF-κB p65 subunit to the nucleus. In conclusion, these findings demonstrate that, in addition to showing promising antidiabetic properties, MA has a direct beneficial effect in cerebral ischemic injury, which may be correlated with the promotion of glutamate clearance by NF-κB-mediated GLT-1 up-regulation.

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