Department of Life Science, College of Agriculture, Tamagawa University, Machida, Tokyo, Japan.
Arch Dermatol Res. 2011 Apr;303(3):171-80. doi: 10.1007/s00403-010-1094-8. Epub 2010 Nov 16.
The aim of the present work was to clarify the anti-melanogenic mechanism of non-steroidal anti-inflammatory drugs (NSAIDs). Mefenamic acid, diclofenac, and nimesulide were used in this study, and these drugs inhibit melanin synthesis in B16F1 melanoma cells. To elucidate the anti-melanogenic mechanism of NSAIDs, we performed western blotting analysis for melanogenic proteins, such as tyrosinase, TRP-1, and TRP-2. All NSAIDs used in this study inhibited tyrosinase protein level. Semi-quantitative RT-PCR analysis showed that the depigmentation effect of mefenamic acid and nimesulide might be due to the inhibition of tyrosinase gene transcription. These results indicate that NSAIDs inhibit α-MSH-enhanced melanin synthesis, and are candidate anti-melanogenic agents since they might be effective in hyperpigmentation disorders.
本研究旨在阐明非甾体类抗炎药(NSAIDs)的抗黑色素生成机制。在本研究中使用了甲芬那酸、双氯芬酸和尼美舒利,这些药物抑制 B16F1 黑色素瘤细胞中的黑色素合成。为了阐明 NSAIDs 的抗黑色素生成机制,我们对黑色素生成蛋白(如酪氨酸酶、TRP-1 和 TRP-2)进行了 Western 印迹分析。本研究中使用的所有 NSAIDs 均抑制酪氨酸酶蛋白水平。半定量 RT-PCR 分析表明,甲芬那酸和尼美舒利的脱色作用可能是由于抑制了酪氨酸酶基因的转录。这些结果表明,NSAIDs 抑制 α-MSH 增强的黑色素合成,并且是候选的抗黑色素生成剂,因为它们可能对色素沉着异常有效。