Skin pigmentation is primarily regulated by melanin production and its accumulation in melanosomes. Hyperpigmentation disorders are commonly treated with agents that inhibit melanin synthesis, such as tyrosinase inhibitors. However, autophagy, a cellular degradation process, has emerged as a potential regulator of pigmentation. Researchers in this study investigated the depigmenting effects of neferine, liensinine, and lotus seed extract (LSE), focusing on their ability to induce autophagy and reduce pigmentation.
Methods
Melanocytes and MelanoDerm tissue models were treated with neferine, liensinine, and LSE to evaluate their effects on melanin accumulation, autophagy activation, and melanosome structure. Transmission electron microscopy (TEM) was used to examine ultrastructural changes in melanocytes, while assays were conducted to assess melanogenesis-related gene expression and tyrosinase activity.
Key Findings
- Depigmentation Mechanism:
- Neferine, liensinine, and LSE reduced melanin content in melanocytes and MelanoDerm without altering melanogenesis-related gene expression or tyrosinase activity.
- Role of Autophagy:
- Increased autophagic flux was observed, indicating that autophagy rather than decreased melanin production caused the reduction in pigmentation.
- TEM images revealed selective degradation of melanosomes through autophagy, with LSE-treated melanosomes displaying structural abnormalities.
- Melanosome-Specific Autophagy:
- LSE-induced autophagy was selective for melanosomes, with autophagosomes containing dark melanosome-like vesicles.
- Melanosomes in LSE-treated cells were often irregular in shape and pigmentation, suggesting impaired melanosome biogenesis and maturation.
This study highlights a depigmentation mechanism, where neferine, liensinine, and LSE induce autophagy, leading to selective melanosome degradation. These findings suggest that LSE not only promotes melanin breakdown but may also impair melanosome biogenesis, making it a promising candidate for cosmetic applications targeting hyperpigmentation.
Further research is warranted to elucidate the molecular pathways involved and explore the potential therapeutic use of LSE for hyperpigmentation disorders.
Link to the study: https://tinyurl.com/2u6zt8rv
