Study on effect and mechanism of salidroside on cognitive ability of Aβ1-40-induced Alzheimer's disease model rats

Abstract

To study the effect and possible impact mechanism of salidroside on cognitive ability of Alzheimer's disease (AD) model rats induced by amyloid beta peptide (Abeta1-40). Abeta1-40 was injected into bilateral hippocampus to create the AD model. Afterwards, different doses of salidroside (25, 50, 75 mg x kg(-1)) were orally administered for 21 days. Rats' learning and memory abilities were detected by Morris water maze testing system. The levels of the superoxide dismutase (SOD), malondialdehyde (MDA), and the expression of nuclear factor-kappaB (NF-kappaB), inducible nitric oxide synthase (iNOS) and receptor for advanced glycation end products (RAGE) protein in hippocampus were also detected by different methods. The place navigation test showed longer escape latency, low frequency of platform quadrant crossing per unit time, damage in learning capacity, significant decrease in SOD acivity in hippocampus, notable increase in MDA content, NF-kappaB, iNOS and RAGE protein expressions in rats. Salidroside (50, 75 mg x kg(-1)) significantly alleviated the impairments of learning and memory ability. The activity of SOD increased in salidroside (50 droside group compared with that of the Alzheimer's disease group (P < 0.01). Salidroside may treat Alzheimer's disease by inhibiting the oxidative stress.