Abstract
Energy metabolism disorders have been shown to exert detrimental effects on the pathology of Alzheimer's disease (AD). The ginsenoside compound K (CK), a major intestinal metabolite underlying the pharmacological actions of orally administered ginseng, has an ameliorating effect against AD, but the relevant molecular mechanism remains unclear. We hypothesized that the improvement of AD by CK is mediated by the energy metabolism signaling pathway induced by amyloid β peptide (Aβ) and tested this hypothesis in HT22 cells. HT22 cells were incubated with CK and exposed to Aβ. Cell viability was analyzed using the MTT assay. Cell growth curves were derived from real-time cell analysis. Apoptosis was determined by flow cytometry, Aβ localization and expression by immunofluorescence, and ATP content by a specific assay kit. The expression of proteins related to the energy metabolism signaling pathway was analyzed using Western blotting. CK treatment improved cell viability, cell growth, and apoptosis induced by Aβ, and the cellular localization and expression of Aβ. Moreover, CK increased ATP content by promoting the activity of glucose transporters (GLUTs). Therefore, the neuroprotective effect of CK against Aβ injury was mainly realized through the activation of the energy metabolism signaling pathway. CK treatment inhibits neuronal damage caused by Aβ through the activation of the energy metabolism signaling pathway, revealing that CK might be one of the key bioactive ingredients of ginseng in the treatment of Alzheimer's disease and may serve as a preventive or therapeutic agent for Alzheimer's disease.
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