Jong-Hwan Lim

Hair loss results from disrupted hair follicle cycling, age-related hormonal imbalance, and oxidative stress, and remains a significant psychological burden for which safe, evidence-based interventions are limited. This study evaluated the effects of a standardized Ageratum conyzoides extract (ACE) on hair follicle growth, hair shaft thickness, and hair shaft morphology in C57BL/6 mice. Mice received oral ACE (10, 20, or 50 mg/kg) for 21 days, and hair regrowth, follicle and shaft characteristics, antioxidant-related responses, serum IGF-1 and VEGF levels, and cuticle morphology were evaluated. ACE accelerated hair regrowth at 20 and 50 mg/kg, increased hair shaft thickness and follicle diameter across all tested doses, and increased follicle number at 20 and 50 mg/kg compared with vehicle, with effects most consistent at 50 mg/kg. ACE upregulated Nrf2, HO-1, SOD2, and GPx1 expression in dorsal skin, increased serum IGF-1 and VEGF levels and dorsal skin superoxide dismutase (SOD) activity, and reduced dorsal skin malondialdehyde (MDA). Scanning electron microscopy revealed reduced hair shaft cuticle damage scores in ACE-treated mice, indicating improved cuticle surface integrity. These findings indicate that ACE promotes hair follicle growth and increases hair shaft thickness, accompanied by increased growth factor levels and enhanced antioxidant status, thereby extending prior findings and supporting further investigation of ACE for hair health.

Background/Objectives: Hair loss, driven by disrupted hair cycles, age-related hormonal imbalances, and oxidative stress, poses significant psychological challenges, necessitating the development of safe and effective therapies. This research investigates the trichogenic potential and underlying mechanisms of a standardized Ageratum conyzoides extract (ACE) using human follicle dermal papilla cells (HFDPCs) and C57BL/6 mice as models. Methods: HFDPCs were treated with ACE to assess its effects on 5α-reductase activity, estrogen receptor (ERα/ERβ) signaling, and activation of Wnt/β-catenin and MAPK pathways. Reactive oxygen species (ROS) levels and antioxidant enzyme expression were also evaluated. In vivo, C57BL/6 mice were administered ACE orally, and hair regrowth, follicle number and depth, and histological changes were measured. Results: In HFDPCs, ACE inhibited 5α-reductase activity, modulated ERα and ERβ signaling, and activated Wnt/β-catenin and MAPK pathways. ACE treatment at 100 μg/mL significantly increased β-catenin, p-GSK3β, and vascular endothelial growth factor (VEGF) expression (p < 0.01) and decreased Dickkopf-related protein-1 (DKK-)1 expression (p < 0.05). It also upregulated VEGF and other hair-growth-related factors and exhibited substantial antioxidant properties by reducing reactive oxygen species (ROS) and elevating the expression of antioxidant enzymes, notably SOD2 at 100 μg/mL. In C57BL/6 mice, oral administration of ACE significantly increased hair regrowth, with the 50 mg/kg group showing the most prominent effects, including increased hair follicle number and depth compared to the negative control group (p < 0.05). These effects were observed to be dose-dependent and comparable to those of minoxidil. Histological analysis confirmed enhanced anagen-phase follicle development. Conclusions: These findings highlight ACE’s multifaceted biological activity in promoting hair growth through hormonal modulation, pathway activation, and antioxidant protection, positioning it as a promising natural supplement for hair growth and health, although further clinical studies are required to confirm its efficacy in humans.