Effects Of Salidroside On PI3-K / AKT Signaling Pathway After Cerebral Ischemia-reperfusion Injury In Rats

Objective To observe the relevance on the mechanism of protective effect of Rhodioloside in cerebral ischemia-reperfusion rats and PI3-K/AKT signaling pathway, and to provide experiment basis of Rhodioloside in preventing and treating cerebral ischemia-reperfusion injury.Methods The male adult Sprague-Dawley rats were randomly divided into three groups:the sham-operation group, the ischemia-reperfusion group(the model group), the Rhodioloside treatment group(10mg/kg). The model of right middle cerebral artery occlusion was established by thread ligation method. The score of the neurological deficit was estimated 2h followed by 24h reperfusion. Histopathological changes were observed by HE staining. The infarct volume was measured using TTC staining. The apoptotic cells were assessed by TUNEL method. The Sprague-Dawley rats received occlusion of the right middle cerebral artery for 2h, and then reperfusion was made for 6h,12h,24h,48h respectively. The expressions of PI3-K, p-AKT and Caspase-3 were evaluated by Western Blotting at different time points.Results1、There was no white cerebral areas, no symptoms of neurological deficit, no histopathology of ischemic injury in the sham group. The score of the neurological deficit in the Rhodioloside treatment group was higher than that of the model group (P<0.01). The infarct volume and the number of apoptotic cells in the Rhodioloside treatment group were all lower obviously than that of the model group (P<0.01). The histopathology of ischemic injury was more improved in the Rhodioloside treatment group than that of the model group.2、The protein expressions of PI3-K and p-AKT in hippocampus at four different time points in model group were obviously higher than that of the sham group (P<0.01).The expressions of PI3-K and p-AKT in model group were gradually increased in 6h after the reperfusion, reached the peak in 24h, and declined in 48h after the reperfusion. The protein expressions of PI3-K and p-AKT in hippocampus at four different time points in Rhodioloside treatment group were obviously higher than that of the model group (P< 0.05),and the trend of protein expression was consistent with the model group at each time point.3、The protein expression of Caspase-3 in hippocampus at four different time points in model group were obviously higher than that of the sham group (P<0.01).The expression of Caspase-3 in model group was gradually increased in 6h after the reperfusion, and reached the peak in 48h. The protein expression of Caspase-3 in hippocampus at four different time points in Rhodioloside treatment group were obviously less than that of the model group (P<0.05),and the trend of protein expression was consistent with the model group at each time point.Conclusion Rhodioloside have a significant neural protection which can reduce brain tissue damage for rats with cerebral ischemia-reperfusion injury. The protective mechanism of Rhodioloside might be associated with activating the PI3-K/AKT signaling pathway and then inhibiting neuronal apoptosis.