Vinegar-Processed Black Soybean Promotes Hair Growth and Prevents Alopecia via Wnt/β-Catenin Pathway.

The escalating prevalence of alopecia, exacerbated by rising life stressors, significantly impacts individuals' physical appearance and psychological well-being, highlighting the need for effective interventions. Black soybean ( [L.] Merr.) is widely used in medicinal and dietary fields with a high safety profile. This study investigated the effects and mechanisms of vinegar-processed black soybean (VPBS) and its aqueous extract (VPBS-AE) on hair regeneration and antialopecia in C57BL/6J mice. For hair regeneration assessment, sodium sulfide-depilated mice were orally administered VPBS (0.75, 1.5, or 3 g·kg·day) or VPBS-AE (0.075, 0.15, or 0.3 g·kg·day) for 18 days. Outcomes were evaluated via trichogram scoring, hair length and weight analysis, histomorphometric evaluation, and Western blot quantification of β-catenin, GSK3β, and Wnt10b expression. To assess antialopecia effects, cyclophosphamide (100 mg·kg) was intraperitoneally administered on Day 9 postdepilation, followed by 6-day oral administration of VPBS (1.5, 3, or 6 g·kg·day) or VPBS-AE (0.15, 0.3, or 0.6 g·kg·day). Alopecia severity was determined through trichogram analysis and macroscopic scoring. Results demonstrated that VPBS dose-dependently accelerated hair growth, stimulated anagen phase entry, and attenuated cyclophosphamide-induced alopecia. VPBS-AE similarly promoted follicular repair, delayed alopecia, and preserved follicle integrity. Western blotting analysis demonstrated that in the model group, sodium hydrosulfide-induced alopecia led to significant downregulation of Wnt10b and β-catenin, and upregulation of GSK-3β. While VPBS-AE treatment effectively restored the expression levels of Wnt10b/β-catenin and suppressed GSK-3β expression, suggesting the therapeutic effects of VPBS-AE may be mediated through the Wnt/β-catenin pathway. Our findings substantiate VPBS and VPBS-AE as promising functional food candidates for hair regeneration and alopecia prevention, with mechanistic insights implicating Wnt/β-catenin signaling modulation.