Autophagy and its regulation by ginseng components

Abstract

Autophagy is the sequential process whereby cell components are degraded, which can occur due to nutrient deprivation. Its regulation has an essential role in many diseases, functioning in both cell survival and cell death. Autophagy starts when mTORC1 is inhibited, resulting in the activation of several complexes to form a cargo that fuses with a lysosome, where it undergoes degradation. In this review, we describe a plant extract that is well known in Korea, namely Korean ginseng extract; we studied how its derivatives and metabolites can regulate autophagy and thus mediate the pathogenesis of certain diseases.

Keywords: Autophagosome; Autophagy; Ginsenosides; Panax ginseng.

Fig. 1

Chemical structure of ginseng components. (A) Ginsenoside Rh2. (B) Ginsenoside F2. (C) Ginsenoside Rb1. (D) Compound K.

Fig. 2

Schematic flow chart of autophagy-mediated molecular targets regarding ginseng components. AMPK, AMP-activated protein kinase; CK, compound K; mTORC1, mammalian target of rapamycin complex 1; PI3KC3, Phosphatidylinositol 3-kinase catalytic subunit type 3; RGE, Red Ginseng extract; ULK1/2, Unc-51 like autophagy activating kinase 1/2.