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

• Published in: Experimental and therapeutic medicine 2014-10, Vol.8 (4), p.1271-1274
• Main Authors: GUO, JINHUI, CHANG, LI, ZHANG, XIN, PEI, SUJUAN, YU, MEISHUANG, GAO, JIANLIAN
• Format: Article
• Language: English
• Subjects: Alzheimer's disease; Amyloid beta-protein; Astrocytes; Autophagy; Biotechnology; Chinese medicine; compound K; Disease; Health aspects; Laboratory animals; Memory; Phosphorylation; Physiological aspects; Proteins; Steroids; Studies; β-amyloid peptides
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2014.1885

The aim of the present study was to investigate the effect of ginsenoside compound K on β-amyloid (Aβ) peptide clearance in primary astrocytes. Aβ degradation in primary astrocytes was determined using an intracellular Aβ 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 Aβ detection. The results demonstrated that compound K promoted the clearance of Aβ 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 Aβ clearance by enhancing autophagy via the mTOR signaling pathway in primary astrocytes.