Neuroprotective effects of salidroside administration in a mouse model of Alzheimer's disease.

Salidroside administration improves memory in different models of learning. However, its influence on models of Alzheimer's disease (AD) has not been widely studied. In the present study, the therapeutic effect of salidroside was investigated in an animal model of AD. APPswe/PS1ΔE9 mouse (n=20) were randomly divided into either the AD model group or the salidroside + AD model group (n=10 in each group), and C57BL/6J mouse (n=20) of identical age and genetic background were randomly divided into either the normal control (NC) group or the salidroside + NC group (n=10 in each group). The Morris water maze behavioral test was applied to all mice in order to investigate the effects of salidroside administration on learning and memory functions. The concentrations of malondialdehyde (MDA), glutathione (GSH) and nitrate in the hippocampus of the mice were determined, and hippocampal superoxide dismutase (SOD) activity was also determined. In addition, terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling was used to investigate the rate of neuronal apoptosis in the hippocampus. Furthermore, the concentrations of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) were tested for in the brain tissues of AD mice. Learning and memory functions in AD mice were revealed to improve following administration of salidroside. Furthermore, salidroside administration was revealed to decrease the concentrations of MDA and nitrate in the hippocampus, decrease the apoptotic rate of hippocampal neurons, and increase the activity of SOD and the concentration of GSH in hippocampal tissue. In addition, it was demonstrated that salidroside administration suppressed the expression levels of IL‑6 and TNF‑α. In conclusion, this study revealed that the administration of salidroside could attenuate the effects of AD‑associated memory and learning impairment in mice. Furthermore, it was demonstrated that the effects of salidroside administration on AD mice were, at least partially, via inhibition of brain oxidative/nitrosative damage, suppression of both IL‑6 and TNF‑α expression levels, and suppression of the hippocampal neuronal apoptotic rate.