Depigmenting mechanism of NSAIDs on B16F1 melanoma cells | Zendy

Kazuomi Sato | Zendy; Hideki Takahashi | Zendy; Masaru Toriyama | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Depigmenting mechanism of NSAIDs on B16F1 melanoma cells

Author(s) -

Kazuomi Sato,

Hideki Takahashi,

Masaru Toriyama

Publication year - 2010

Publication title -

archives of dermatological research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.776

H-Index - 80

eISSN - 1432-069X

pISSN - 0340-3696

DOI - 10.1007/s00403-010-1094-8

Subject(s) - tyrosinase , microphthalmia associated transcription factor , nimesulide , mefenamic acid , melanin , pharmacology , chemistry , hyperpigmentation , kojic acid , mechanism of action , melanoma , blot , biochemistry , medicine , in vitro , gene , enzyme , cancer research

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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research