Objective  To investigate the influence of salidroside on inflammatory factors of model rats with Alzheimer′s disease induced by scopolamine.

  Methods  A total of 40 male SD rats were randomly divided into blank group, model group and high-, medium- and low-dose salidroside groups. Model rats with Alzheimer′s disease were established by intraperitoneal injection of scopolamine. The blank group and model group were given normal saline with the dose of 10 mL/(kg·d), and the high, medium and low dose groups were given 75, 50 and 25 mg/(kg·d) salidroside (salidroside powder with purity >95% should be mixed with double distilled water) for 21 days. The results of behavioral experiment, pathological experiment and ELISA experiment were compared.

  Results  Morris water maze test showed that on the second day of the experiment, the action track of the high-dose group was similar to that of the blank group, and the memory ability of the rats to the platform position was better than that of the model group; the ratio of target platform quadrant search time and times of crossing platform in the high-dose group were significantly higher than those in the model group, and the latency time in the model group was significantly longer than that in the medium-dose group (P < 0.05). HE staining showed that the cell morphology of the high-dose group was roughly similar to that of the blank group, and the nerve cells were generally thin and arranged regularly; hippocampal neurons in the model group were significantly damaged and scattered. Compared with the blank group, the brain tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the model group were significantly higher (P < 0.05); compared with the model group, brain TNFα and IL-1β levels in high-dose group and medium-dose group were significantly lower (P < 0.05).

  Conclusion  Salidroside can significantly enhance the learning and memory abilities of AD rats, reduce the damage of hippocampal neurons, regulate the central inflammatory state, and repair the pathological damage of hippocampal neurons, and its mechanism may be related to improvement of inflammatory response and enhancement of immune function.