Ginsenoside compound K promotes β-amyloid peptide clearance in primary astrocytes via autophagy enhancement

The aim of the present study was to investigate the effect of ginsenoside compound K on beta-amyloid (A beta) peptide clearance in primary astrocytes. A beta degradation in primary astrocytes was determined using an intracellular A beta clearance assay. Aggregated LC3 in astrocyte cells, which is a marker for the level of autophagy, was detected using laser scanning confocal microscope. The effect of compound K on the mammalian target of rapamycin (mTOR)/autophagy pathway was determined using western blot analysis, and an enzyme-linked immunosorbent assay was used for A beta detection. The results demonstrated that compound K promoted the clearance of A beta and enhanced autophagy in primary astrocytes. In addition, it was found that phosphorylation of mTOR was inhibited by compound K, which may have contributed to the enhanced autophagy. In conclusion, compound K promotes A beta clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.