Abstract

Objective To investigate the effect of salidroside on brain edema and neurological function in global cerebral ischemia-reperfusion injury in rats.Methods A total of 100 Sprague Dawley rats were randomly divided into sham operation,ischemia-reperfusion and salidroside 12,24 and 48 mg/kg groups （n =20 in each group）,and than redivided into 6 h,24 h,72 h and 7 dsubgroups （n =5 in each subgroup）.A rat model of global cerebral ischemia was established using the four-vessel occlusion method.Immediately after modeling,all groups were administered intragastrically for 7 days.The brain water content was quantitated by the wet-dry weight method.The neurological evaluation was performed using a neurological deficit score （NDS）.Results After modeling both the ischemia-reperfusion group and all the salidroside groups had significant neurological deficit,and as time went by,it was improved gradually.Compared to the ischemia-reperfusion group at the corresponding time points,neurological deficit in all the salidroside groups was improved significantly （all P 〈 0.05）,and showing a dose-dependent trend.Compared to the salidroside 12 mg/kg and 24 mg/kg groups,neurological deficit in the salidroside 48 mg/kg group was improved significantly at 72 hours and 7 days （all P 〈 0.05）.The brain water contents began to increase at 6 hours after modeling in the the ischemia-reperfusion group and all the salidroside group.They reached the peak at 72 hours,and significantly higher than that in the sham operation group （all P 〈 0.05）.The brain water contents in all the salidroside group were significantly lower than those in the ischemiareperfusion group at 24 and 72 hours after modeling （all P 〈 0.05） and showing a dosedependent trend.The brain water content in the salidroside 48 mg/kg group was close to that in the sham operation group at 7 days after modeling.Conclusions Salidroside may significantly decrease brain edema and improve neurological function in global cerebral ischemia-reperfusion injury in rats,and it has a neuroprotective effect. Key words: Rhodioloside; Brain ischemia; Disease models, animal; Brain edema; Neuroprotective agents; Rats

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