Forty SD rats were randomly divided into control group， model group， positive drug group， and DST group， with 10 rats in each group. Except for control group， the rats in other groups were given intraperitoneal injection of D-gal at a dose of 500 mg·kg^－1·d^－1 for 40 d to establish the aging models. On the 5th day of the model construction， the rats in positive drug group was given vitamin E 0.027 g·kg^－1， and the rats in DST group were given DST 5mL （equivalent to 0.3 g·kg^－1·d^－1 crude drug）， for 36 d. The states of the rats were observed and the growth curves were draw； the water maze was used to detect the learning and memory abilities of the rats； the biochemical and ELISA kits were used to detect the activities of SOD， GSH and the levels of MDA and cAMP in the rat brain tissue； the transmission electron microscope was used to observe the ultrastructures of the rat hippocampus neurons； Congo red staining was used to observe the age spots in hippocampus tissue of the rats； Western blotting was used to detect the expression levels of cAMP/PKA/CREB signaling pathway-related proteins in hippocampus tissue of the rats.

Compared with model group， the body weights of rats in positive drug group and DST group were increased， the learning and memory abilities were increased （P<0.05）， the activities of SOD and GSH and the levels of cAMP in brain tissue of the rats were significantly increased（P<0.05），and the levels of MDA were decreased （P<0.05）. Compared with model group， the pathological changes of neuron ultrastructures of the rats in positive drug group and DST group were improved and the areas of orange-red sediments and age spots in hippocampus tissue of the aging model rats were significantly decreased（P<0.01）；the expression levels of PKA， cAMP， adenylate cyclase（ADCY），CREB，and brain-derived neurotrophic factor （BDNF） proteins in brain tissue of the rats were significantly increased（P<0.05），and the expression levels of guanine nucleotide-binding protein alpha inhibitor（GNAI） were decreased （P<0.05）.

DST can significantly improve the cognitive ability of the D-gal-induced aging model rats，and its mechanism may be related to scavenging free radicals and activating cAMP/PKA/CREB signaling pathway to improve the nerve cell damage.