LAUSR

We examined the effects of salidroside on cognition in rats with vascular dementia and explored the mechanisms of its neuroprotective effects. Sprague-Dawley rats ( n =60) were randomly subdivided into 3 equal groups: controls, untreated rats with vascular dementia, and rats with vascular dementia treated with salidroside (30 mg/kg for 8 weeks). Vascular dementia was provoked by bilateral occlusion of the common carotid arteries. The cognitive function was tested in the Morris water maze. Oxidation stress was assessed by the levels of superoxide dismutase and malondialdehyde assayed with standard biochemical kits. Expressions of proteins p38, p-p38, and caspase-3 were assessed by Western blotting. In untreated rats with vascular dementia, the cognitive function degraded in parallel with a decrease in superoxide dismutase, malondialdehyde accumulation, and activation the expression of p-p38 and caspase-3. Salidroside treatment significantly improved the cognitive functions in rats with vascular dementia and diminished adverse shifts in the levels of superoxide dismutase and malondialdehyde as well as the changes in the expression of p-p38 and caspase-3 in comparison with similar changes in untreated rats. Moreover, salidroside improved spatial learning and memory in rats with vascular dementia. The therapeutic effect of salidroside is probably based on its antioxidant effects and inhibition of caspase-3-mediated apoptosis via suppression of p38 MAPK signaling pathway.