Objective: To investigate the effect of forsythiaside on scopolamine-induced learning and memory impairment in mice

and explored the possible mechanism. Method: Kunming mice were randomly divided into 4 groups (n=12 per group):normal group

scopolamine model group (3 mg·kg-1)

positive control group (donepezil

3 mg·kg-1)

and forsythiaside group (200 mg·kg-1). All groups were administered with drugs by gastric gavage for 2 weeks. On the 14th day

scopolamine model group

donepezil group and forsythiaside group were intraperitoneally injected with scopolamine (3 mg·kg-1). 20 min later

the step-down passive avoidance test was performed to evaluate the effect of forsythiaside on AchE and CAMP-extracellular signal-regulated kinase pathway. For another experiment

Kunming mice were randomly divided into 4 groups (n=8 per group):normal group

scopolamine model group (3 mg·kg-1)

positive control group (Vit E

100 mg·kg-1)

forsythiaside group (200 mg·kg-1). After 14 days

all mice were beheaded to detect the effect of forsythiaside on superoxide dismutase(SOD)

malondialdehyde(MDA) and monoamine oxidase(MAO). Result: Significant effects were observed in the step-down passive avoidance test in the acquisition and consolidation periods. Forsythiaside can increase the reduced safe platform time ratio in the scopolamine group (P<0.05). Forsythiaside can decrease the AchE activity in the cortex and hippocampus

increase the expression of p-ERK in hippocampus (P<0.05)

with statistically significant differences compared with model group. Compared with the model group

scopolamine can reduce SOD

MDA and MAO content in cortex and hippocampus (P<0.05). Forsythiaside can significantly increase SOD

MDA and MAO content in cortex and hippocampus

with significant differences compared with scopolamine group (P<0.05). Conclusion: Forsythiaside ameliorated scopolamine-induced learning and memory impairment by modulating AchE activity

cAMP expression and p-ERK and resisting oxidation.