Umbelliferone stimulated melanogenesis and increased glutathione level in B16F10 cells

• Published in: Toxicology and environmental health sciences 2017-06, Vol.9 (2), p.152-160
• Main Authors: Lee, Yunjung, Ku, Bonhee, Kim, Dongsoo, Choi, Eun-Mi
• Format: Article
• Language: English
• Subjects: Biomedical and Life Sciences; Biomedicine; Disorders; Environmental Health; Formulas (mathematics); Glutathione; JNK protein; Kinases; MAP kinase; Melanin; Melanocyte-stimulating hormone; Melanoma; Microphthalmia-associated transcription factor; Original Article; Oxidation; Pharmacology/Toxicology; Proteins; Skin; Tanning; Toxicity; Tyrosinase; Tyrosinase-related protein 1; Ultraviolet radiation; Umbelliferone
• ISSN: 2005-9752; 2233-7784
• DOI: 10.1007/s13530-017-0316-2

Umbelliferone (7-hydroxycoumarin) treatment caused an increase in melanin content in B16F10 melanoma cells in a dose-dependent manner, without causing toxicity. The increase in melanin content was correlated with increases in the activity of tyrosinase, the rate-limiting enzyme in melanin synthesis, and the expressions of melanogenic proteins, including tyrosinase, tyrosinase-related protein 1, and microphthalmia-associated transcription factor, the master transcriptional regulator for melanogenesis. Unlike α-melanocyte-stimulating hormone, umbelliferone did not cause melanogenesis-associated oxidation and depletion of glutathione. Conversely, umbelliferone treatment resulted in a significant and dose-dependent increase in glutathione. Umbelliferone caused activation of JNK, p38 MAPK, and GSK3β in a dose- dependent manner, suggesting possible involvement of those protein kinases in umbelliferone-induced stimulations of melanogenesis and antioxidant system. Our results suggest that umbelliferone stimulates both melanogenesis and antioxidant defense, providing more effective protection against UV-induced photodamage. They also imply possible applications of umbelliferone in self-tanning and treatment of skin disorders related with melanin deficiency.