Ginkgobiloba extract protects diabetic rats against cerebral ischemia‑reperfusion injury by suppressing oxidative stress and upregulating the expression of glutamate transporter 1.

Abstract

The current study aimed to evaluate the neuroprotective effect of Ginkgo biloba extract (GbE) on the progression of acute cerebral ischemia-reperfusion injury in diabetic rats, and to determine the molecular mechanism associated with this effect. Streptozotocin (STZ) induced diabetic rats were pretreated with GbE (50, 100 and 200 mg/kg/day; intragastric) for 3 weeks. During this period, body weight changes and fasting blood glucose levels were assessed each week. Following pretreatment, rats were subjected to suture occlusion of the middle cerebral artery for 30 min, which was followed by 24 h of reperfusion. Neurological deficits were subsequently evaluated at 2 and 24 h following reperfusion. Rats were sacrificed after 24 h reperfusion, and infarct volume and S100B content were measured to evaluate the neuroprotective effect of GbE. The results of the present study demonstrated that GbE pretreatment improved neurological scores, and reduced cerebral infarct volume and S100B content. Oxidative stress markers, including glutathione (GSH) and superoxide dismutase (SOD) were increased, and malondialdehyde (MDA) contents were reduced following GbE treatment. The levels of p-Akt, p-mTOR and glutamate transporter 1 (GLT1) were observed to be increased in GbE-pretreated rats. These results indicated that GbE pretreatment may serve a protective role against cerebral ischemia-reperfusion injury in diabetic rats by inhibiting oxidative stress reaction, upregulating the expression of Akt/mTOR and promoting GLT1 expression. In conclusion, the current study revealed the protective role and molecular mechanisms of GbE in diabetic rats with cerebral ischemia-reperfusion injury, and may provide novel insight into the future clinical treatment of this condition.