Ginsenoside compound K ameliorates Alzheimer's disease in HT22 cells by adjusting energy metabolism

摘要

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 beta peptide (A beta) and tested this hypothesis in HT22 cells. HT22 cells were incubated with CK and exposed to A beta. Cell viability was analyzed using the MTT assay. Cell growth curves were derived from real-time cell analysis. Apoptosis was determined by flow cytometry, A beta 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 A beta, and the cellular localization and expression of A beta. Moreover, CK increased ATP content by promoting the activity of glucose transporters (GLUTs). Therefore, the neuroprotective effect of CK against A beta injury was mainly realized through the activation of the energy metabolism signaling pathway. CK treatment inhibits neuronal damage caused by A beta 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.