Ginsenoside CK inhibits androgenetic alopecia by regulating Wnt/β‐catenin and p53 signaling pathways in AGA mice

Abstract

Abstract Androgenetic alopecia (AGA) is one of the most common chronic skin diseases caused by the destruction of androgens in the body. It is caused by the excessive deposition of dihydrotestosterone around the hair follicle, resulting in hair follicle atrophy and hair cell apoptosis. It causes great anxiety and psychological distress to patients and affects sexual function in severe cases. As traditional Chinese herbs, ginsenosides have been proven to possess various pharmacological activities. Ginsenoside CK is one of the main ginsenosides, but its role and molecular mechanism in treating AGA remain unclear. Here, we found that ginsenoside CK intervention significantly reduced back hair loss in AGA mice, improved sexual organ damage and hair follicle cell apoptosis, and promoted hair growth in AGA mice. Ginsenoside CK treatment inhibited p53 expression, reduced the apoptosis of hair follicle cells induced by hormone deposition, activated the Wnt/β‐catenin cell proliferation signaling pathway, increased the level of vascular endothelial growth factor, promoted cell proliferation, and improved the atrophy of hair follicle tissue. Ginsenoside CK treatment also reduced testosterone levels in AGA mice, improved testicular tissue inflammation, and restored normal hormone metabolism in AGA mice. Our results indicated that ginsenoside CK reduced hair follicle cell apoptosis, promoted proliferation and development, and prolonged the hair growth cycle by regulating the Wnt and p53 signaling pathways, indicating the potential value of ginsenoside CK as a natural therapeutic agent for AGA.

Keywords

• AGA
• DHT
• Ginsenoside CK
• p53
• Wnt/β‐catenin signaling pathway