Objective To observe the effect of acanthopanax refined polysaccharide (ASPS) on nicotine-induced learning and memory impairment in mice.

Methods A total of 48 male mice and 48 females at 6 weeks of age were selected and were divided into two batches for animal experiments: the Morris and the new object recognition batch. Each batch was randomly divided into 6 groups according to body weight: blank control group, model group, drug positive group, high-dose ASPS group, medium-dose ASPS group, and low-dose ASPS group. Except for the blank group, the remaining 5 groups were injected subcutaneously with 0.5mg/kg of nicotine every day for 7 days to prepare a nicotine memory disorder model. After 24 hours of injection of nicotine at the 7^th day, the drug positive group was gavaged piracetam for 800 mg/kg, and the high-dose, medium-dose and low-dose ASPS groups were gavaged for 270, 90 and 30 mg/kg of ASPS respectively for 7 days. The learning and memory ability of mice was detected by water maze test and new object recognition test, respectively. After the two tests, superoxide dismutase(SOD) activity in serum and 5-Hydroxytryptamine (5-HT) content in hippocampal tissue were detected.

Results The results of new object recognition experiment showed that the discrimination indexes of the high-, medium- and low-dose ASPS groups were significantly higher than that of the model group (P < 0.01 or P < 0.05). The results of water maze experiment showed that the time to find the platform in the spatial search experiment was significantly shorter in the high- and medium-dose ASPS groups than that in the model group (P < 0.05). In the positioning voyage test, the number of mouse platform entries in the high-dose ASPS group was significantly more than that in the model group (P < 0.05); the proportions of Ⅲ quadrant routes in the high-and medium-dose ASPS groups were higher than those in the model group (P < 0.05). The high-, medium- and low-dose ASPS groups were significantly higher than those in the model group (P < 0.01); the determination of hippocampal tissue content in mice showed that the content of 5-HT in the high- and medium-dose ASPS groups was significantly higher than that in the model group (P < 0.01 or P < 0.05).

Conclusion ASPS can significantly improve the learning and memory ability of nicotine-quitting mice, relieve the damage of hippocampal neurotransmitters, and regulate oxidative stress in vivo. The mechanism may be related to improving the body's antioxidant capacity and regulating hippocampal neurotransmitter levels.