590纳米发光二极管光调制通过上调抗氧化酶过氧化氢酶来降低紫外线A诱导的金属蛋白酶-1表达。
LED 590 nm photomodulation reduces UVA-induced metalloproteinase-1 expression via upregulation of antioxidant enzyme catalase.
作者信息
Lan Cheng-Che E, Ho Pei-Yun, Wu Ching-Shuang, Yang Rei-Cheng, Yu Hsin-Su
机构信息
Department of Dermatology, Kaohsiung Medical University Hospital, and Department of Dermatology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Dermatology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Department of Dermatology, Kaohsiung Medical University Hospital, and Department of Dermatology, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
出版信息
J Dermatol Sci. 2015 May;78(2):125-32. doi: 10.1016/j.jdermsci.2015.02.018. Epub 2015 Mar 5.
BACKGROUND
Light at visible spectrum has been associated with anti-inflammatory and anti-aging effects. Ultraviolet A (UVA) radiation is the most important environmental factor associated with exogenous aging via induction of reactive oxygen species (ROS).
OBJECTIVE
In this study, we focused on elucidating the molecular mechanisms involved in biological effects associated with 590 nm light delivered from light emitting diode (LED).
METHODS
UVA-induced metalloproteinase-1 (MMP-1) expression in dermal fibroblast was used as a model system for investigation.
RESULTS
Pretreating cultured human fibroblasts with 590 nm light attenuated UVA-induced ROS, phosphorylated Jun N-terminal kinases, and MMP-1 expressions in a sequential manner. Pretreatment with potent antioxidant N-acetylcysteine produced similar effect, suggesting enhanced antioxidant capacity induced by 590 nm photomodulation. Further experiments demonstrated that 590 nm photomodulation attenuated UVA-induced ROS and MMP-1 expressions via mitochondrial retrograde signaling that augments the antioxidant enzyme expression in a peroxisome proliferators-activated receptor γ coactivator-1α-dependent manner.
CONCLUSION
Our results provided possible mechanistic insights explaining the effect of visible light on treating clinical conditions associated with ROS-mediated dysfunctions.
背景
可见光谱中的光具有抗炎和抗衰老作用。紫外线A（UVA）辐射是通过诱导活性氧（ROS）与外源性衰老相关的最重要环境因素。
目的
在本研究中，我们专注于阐明与发光二极管（LED）发出的590nm光相关的生物学效应所涉及的分子机制。
方法
将UVA诱导的真皮成纤维细胞中金属蛋白酶-1（MMP-1）的表达用作研究的模型系统。
结果
用590nm光预处理培养的人成纤维细胞可依次减弱UVA诱导的ROS、磷酸化的Jun N末端激酶和MMP-1的表达。用强效抗氧化剂N-乙酰半胱氨酸预处理产生了类似的效果，表明590nm光调制诱导了抗氧化能力增强。进一步的实验表明，590nm光调制通过线粒体逆行信号传导减弱了UVA诱导的ROS和MMP-1表达，该信号传导以过氧化物酶体增殖物激活受体γ共激活因子-1α依赖性方式增强抗氧化酶表达。
结论
我们的结果提供了可能的机制见解，解释了可见光对治疗与ROS介导的功能障碍相关的临床病症的作用。
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