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Salidroside prevents cognitive impairment induced by chronic cerebral hypoperfusion in rats
Zhi-Qiang Yan1, Jun Chen2, Guo-Xiang Xing3
1Department of Neurosurgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China Department of Neurosurgery, Urumqi General Hospital of Lanzhou Military Command, Urumqi, China.
Objective:
To investigate the effects of salidroside on cognitive dysfunction induced by chronic cerebral hypoperfusion in rats.
Methods:
Male Sprague-Dawley rats (n = 36) were divided into three groups (n = 12 per group): sham operation; bilateral permanent occlusion of the common carotid arteries (2-VO); 2-VO + salidroside. Rats received 20 mg/kg per day salidroside or vehicle intraperitoneal injection beginning the day before surgery and continuing until 34 days postoperatively. Cognitive function was evaluated by Morris water maze test and hippocampal long-term potentiation (LTP) measurement. Hippocampal neuronal apoptosis was evaluated via immunofluorescence.
Results:
Chronic cerebral hypoperfusion caused marked cognitive deficit and LTP inhibition. These effects were largely ameliorated by salidroside administration. Salidroside prevented caspase-3 activation, increased the ratio of Bax/Bcl-2, and reversed hippocampal neuronal loss induced by chronic cerebral hypoperfusion.
Conclusions:
Salidroside prevents cognitive deficits caused by chronic cerebral hypoperfusion in rats, and alleviates apoptosis in the hippocampal CA1 area.
