Abstract
Kami-ondam-tang (KOT), a traditional Chinese medicine, has been used to treat mental and neuropsychiatric disorders, including dementia. This study aimed to investigate the effects of KOT on cognition and the mechanisms underlying these effects in mice. Using the passive avoidance task, we investigated the effect of sub-chronic administration of KOT on the cognition of mice. We also examined the expressions of protein kinase B (Akt), cAMP response element-binding protein (CREB), brain-derived neurotrophic factor (BDNF), and doublecortin (DCX) in the hippocampal CA1 and dentate gyrus regions using immunohistochemistry and western blotting. The administration of KOT (50mg/kg/day, p.o.) for 14 days significantly increased step-through latency in the passive avoidance task compared with vehicle-treated controls. Furthermore, KOT administration (50mg/kg/day, p.o.) significantly increased the expressions of phosphorylated Akt, phosphorylated CREB and BDNF in the hippocampal CA1 and dentate gyrus. In addition, KOT administration resulted in a significant increase in the number of DCX-immunopositive cells in the dentate gyrus. These results suggest that KOT enhances cognitive performance through the upregulation of Akt-CREB-BDNF signaling and neurogenesis.
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