RESUMO
Objective To explore the mechanism of protective effect of Rhodioloside in cerebral ischemia-reperfusion rats and its relevance to phosphatidylinositol 3-kinases ( PI3-K)/protein serine-threonine kinases ( AKT) signaling pathway .Methods Forty eight Sprague-Dawley rats were randomly divided into four groups: sham-operation group , ischemia-reperfusion group , and Rhodiolo-side treatment groups (5 and 10 mg/kg).The model of right middle cerebral artery occlusion was established with thread ligation meth -od.The score of the neurological deficit was estimated 2 h followed by 24 h reperfusion.Histopathological changes were observed by hematoxylin-eosin(HE) staining.The infarct volume was measured with triphenyltetrazolium chloride (TTC) staining.Apoptotic cells were assessed with terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) method.The expressions of PI3-K and p-AKT were evaluated with immunohistochemistry .Results The score of the neurological deficit was decreased more ob-viously, the number of apoptotic were decreased more significantly , the expressions of PI3-K and p-AKT were increased more signifi-cantly in the Rhodioloside treatment groups (5 and 10 mg/kg) than in the ischemia-reperfusion group ( P <0.05).The score of the neurological deficit was decreased , the number of apoptotic was decreased , and the expressions of PI 3-K and p-AKT were increased in the Rhodioloside treatment group (10 mg/kg) than the Rhodioloside treatment group (5 mg/kg) ( P <0.05).Conclusions The protective mechanism of Rhodioloside therapy against cerebral ischemia r-eperfusion injury might be associated with activating the PI 3-K/AKT signaling pathway and then inhibiting neuronal apoptosis .