Neuroprotection of Maslinic Acid, a Novel Glycogen Phosphorylase Inhibitor, in Type 2 Diabetic Rats

Abstract

Aim To investigate the effects of maslinic acid (MA), a novel glycogen phosphorylase inhibitor in hyperglycemic rats after cerebral ischemia/reperfusion injury. Methods Rats were fed with high fat diet (HFD) followed by low-dose streptozotocin (STZ) injection to induce metabolic syndrome. Three doses of MA (10, 5 and 2.5 mg·kg −1·d −1) were administered once daily by i.g. for 2 weeks. Neurological outcomes were compared in vehicle and MA treated HFD/STZ rats with cerebral ischemia/reperfusion injury induced by bilateral common carotid artery occlusion. Results The elevation of plasma fasting glucose (GLU), serum plasma triglyceride (TG) and plasma total cholesterol (TC) was antagonized by MA significantly. Cerebral ischemia with pre-existing hyperglycemia and hyperlipemia caused prominent elevation in MDA levels and decrease in SOD activity. Extensive neuronal death occurred in the CA1 area of hippocampus at day 3 after forebrain ischemia. MA significantly attenuated ischemia-induced neuronal death in a dose-dependent manner. Moreover, MA caused a significant reduction in MDA levels and elevation in SOD activity in both cortex and hippocampus. Conclusion Results suggested the prophylaxis of MA may also show beneficial effects in reducing cerebral damage after stroke for patients with type 2 diabetes.