福司可林可保护角质形成细胞免受紫外线B诱导的细胞凋亡，并增强DNA修复能力，且与其对黑素生成的影响无关。
Forskolin protects keratinocytes from UVB-induced apoptosis and increases DNA repair independent of its effects on melanogenesis.
作者信息
Passeron Thierry, Namiki Takeshi, Passeron Hélène J, Le Pape Elodie, Hearing Vincent J
机构信息
Pigment Cell Biology Section, Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
出版信息
J Invest Dermatol. 2009 Jan;129(1):162-6. doi: 10.1038/jid.2008.182. Epub 2008 Jun 26.
Abstract
Melanin pigments provide efficient protection against ultraviolet B (UVB) radiation but DNA repair also plays a key role in eliminating UV-induced damage and preventing the development of skin cancers. In this study, we demonstrate that forskolin (FSK), an agent that increases intracellular levels of cAMP, protects keratinocytes from UVB-induced apoptosis independently from the amount of melanin in the skin. FSK enhances the removal of the two major types of UVB-induced DNA damage, cyclobutane pyrimidine dimers and 6,4-photoproducts, by facilitating DNA repair. These findings suggest new preventive approaches with topical formulations of FSK or other bioactive agents that could be applied to the skin before sun exposure to increase its ability to repair DNA damage.
摘要
黑色素能够有效抵御紫外线B（UVB）辐射，但DNA修复在消除紫外线诱导的损伤以及预防皮肤癌发生方面也起着关键作用。在本研究中，我们证明了福斯高林（FSK），一种可提高细胞内cAMP水平的物质，能够独立于皮肤中黑色素的含量，保护角质形成细胞免受UVB诱导的凋亡。FSK通过促进DNA修复，增强了对两种主要类型的UVB诱导的DNA损伤，即环丁烷嘧啶二聚体和6,4 - 光产物的清除。这些发现提示了新的预防方法，即使用FSK或其他生物活性剂的局部制剂，在阳光照射前涂抹于皮肤，以增强其修复DNA损伤的能力。
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