Depigmenting mechanism of NSAIDs on B16F1 melanoma cells
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- 作者：Kazuomi Sato (1) kzsato@agr.tamagawa.ac.jp
Hideki Takahashi (2)
Masaru Toriyama (2) - 关键词：Non ; steroidal anti ; inflammatory drugs (NSAIDs) – ; Melanogenesis – ; Tyrosinase – ; Microphthalmia ; associated transcription factor (Mitf) – ; B16F1 melanoma
- 刊名：Archives of Dermatological Research
- 出版时间：April 2011
- 出版年：2011
- 期刊代码：14_0340-3696
- 类别：med
- 卷：303
- 期：3
- 页码：171-180
- 数据来源：sp
摘要
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.