Hair-Growth Potential of Ginseng and Its Major Metabolites: A Review on Its Molecular Mechanisms

Abstract

The functional aspect of scalp hair is not only to protect from solar radiation and heat/cold exposure but also to contribute to one's appearance and personality. Progressive hair loss has a cosmetic and social impact. Hair undergoes three stages of hair cycle: the anagen, catagen, and telogen phases. Through cyclical loss and new-hair growth, the number of hairs remains relatively constant. A variety of factors, such as hormones, nutritional status, and exposure to radiations, environmental toxicants, and medications, may affect hair growth. Androgens are the most important of these factors that cause androgenic alopecia. Other forms of hair loss include immunogenic hair loss, that is, alopecia areata. Although a number of therapies, such as finasteride and minoxidil, are approved medications, and a few others (e.g., tofacitinib) are in progress, a wide variety of structurally diverse classes of phytochemicals, including those present in ginseng, have demonstrated hair growth-promoting effects in a large number of preclinical studies. The purpose of this review is to focus on the potential of ginseng and its metabolites on the prevention of hair loss and its underlying mechanisms.

Keywords: BMP/Smad; Shh/Gli; TGF-β; WNT/β-catenin; ginseng; human-hair-follicle dermal papilla cells; mouse-hair growth.

Figure 1

Potential molecular targets of ginseng in hair growth and loss. Ginseng exhibits therapeutic potential for hair growth and preventing hair loss by preventing the apoptosis of dermal follicle papilla cells. Ginseng components: RGE (red ginseng extract), RGO (red ginseng oil), ginsenoside Rd, Rb1, Rh2, Rg1, Rg3. antiandrogenic: DHT (dihydrotestosterone), 5-aR (5α-reductase). Apoptosis inhibition: TGF-β (transforming growth factor beta), Smads (homologues of the Drosophila protein, mothers against decapentaplegic (Mad) and the Caenorhabditis elegan sprotein Sma). Proliferation activation: WNT (wingless-type MMTV integration site family member), Shh (Sonic hedgehog), Gli (glioma-associated oncogene homolog), VEGF (vascular endothelial growth factor), EGF (epidermal growth factor), AKT/PKB (protein kinase B), ERK (extracellular-signal-regulated kinases).