Barolet Augustin C, Magne Brice, Ferland Karel, Uzunbajakava Natallia E, Barolet Daniel, Germain Lucie
Regenerative Medicine Division, CHU de Quebec - Université Laval Research Centre, Quebec City, QC, Canada.
Centre de recherche en organogénèse expérimentale de l'Université Laval (LOEX), Université Laval, Quebec City, QC, Canada.
Front Physiol. 2025 Jan 9;15:1513054. doi: 10.3389/fphys.2024.1513054. eCollection 2024.
Recent findings show that visible light, particularly blue light, stimulates melanogenesis in human skin, though the underlying mechanisms remain debated. This study aimed to determine the cell damage threshold of non-ionizing blue light on keratinocytes while preserving their ability to stimulate melanogenesis.
Human keratinocytes (N = 3) and melanocytes (N = 3) were isolated from skin samples of varying Fitzpatrick skin phototypes and irradiated with blue light (λpeak = 457 nm) and UVA light (λpeak = 385 nm). Cellular metabolic activity was assessed using the AlamarBlue HS assay, α-Melanocyte-Stimulating Hormone (α-MSH) production by keratinocytes was quantified using ELISA, and Western blotting was used to assess pro-melanogenic factor expression in melanocytes.
High blue light intensity (50 mW/cm, 50 J/cm) and UVA light (15 mW/cm, 20 J/cm) significantly reduced cellular metabolic activity, with a 0.86 ± 0.055 and 0.60 ± 0.031 (mean ± SD) fold decrease compared to their respective sham by day 7. In contrast, moderate blue light intensities (5-15 mW/cm, 10-20 J/cm) preserved cellular metabolic activity while stimulating α-MSH production, with an optimal balance achieved at 10 mW/cm, 15 J/cm (1.14 ± 0.046 fold increase relative to sham on day 7). Co-culture experiments confirmed that irradiated keratinocytes enhanced melanogenesis in melanocytes via paracrine signaling, increasing the expression of Tyrosinase and Dopachrome Tautomerase (DCT). Direct blue light irradiation on melanocytes also increased pigmentation without significant cellular damage.
Moderate-intensity blue light at 10 mW/cm, 15 J/cm effectively stimulates melanogenesis while maintaining cellular metabolic activity in both keratinocytes and melanocytes, offering a promising, safe approach for blue light therapies targeting pigmentation disorders.
最近的研究结果表明，可见光，尤其是蓝光，会刺激人体皮肤中的黑色素生成，但其潜在机制仍存在争议。本研究旨在确定非电离蓝光对角质形成细胞的细胞损伤阈值，同时保留其刺激黑色素生成的能力。
从不同菲茨帕特里克皮肤光类型的皮肤样本中分离出人角质形成细胞（N = 3）和黑素细胞（N = 3），并用蓝光（λ峰值 = 457nm）和紫外线A光（λ峰值 = 385nm）照射。使用AlamarBlue HS检测法评估细胞代谢活性，使用酶联免疫吸附测定法（ELISA）对角质形成细胞产生的α-黑素细胞刺激激素（α-MSH）进行定量，并使用蛋白质印迹法评估黑素细胞中促黑素生成因子的表达。
高强度蓝光（50mW/cm，50J/cm）和紫外线A光（15mW/cm，20J/cm）显著降低细胞代谢活性，到第7天时，与各自的假照射相比，分别下降了0.86±0.055倍和0.60±0.031倍（平均值±标准差）。相比之下，中等强度蓝光（5-15mW/cm，10-20J/cm）在刺激α-MSH产生的同时保留了细胞代谢活性，在10mW/cm，15J/cm时达到最佳平衡（相对于第7天的假照射增加了1.14±0.046倍）。共培养实验证实，经照射的角质形成细胞通过旁分泌信号增强黑素细胞中的黑色素生成，增加酪氨酸酶和多巴色素互变异构酶（DCT）的表达。直接对黑素细胞进行蓝光照射也增加了色素沉着，而没有明显的细胞损伤。
10mW/cm，15J/cm的中等强度蓝光有效地刺激了黑色素生成，同时维持了角质形成细胞和黑素细胞的细胞代谢活性，为针对色素沉着紊乱的蓝光疗法提供了一种有前景的安全方法。
