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Ursolic acid inhibits pigmentation by increasing melanosomal autophagy in B16F1 cells
- Source :
- Biochemical and Biophysical Research Communications. 531:209-214
- Publication Year :
- 2020
- Publisher :
- Elsevier BV, 2020.
-
Abstract
- Melanosomes are specialized membrane-bound organelles that are involved in melanin synthesis. Unlike melanosome biogenesis, the melanosome degradation pathway is poorly understood. Among the cellular processes, autophagy controls degradation of intracellular components by cooperating with lysosomes. In this study, we showed that ursolic acid inhibits skin pigmentation by promoting melanosomal autophagy, or melanophagy, in melanocytes. We found that B16F1 cells treated with ursolic acid suppressed alpha-melanocyte stimulating hormone (α-MSH) stimulated increase in melanin content and activated autophagy. In addition, we found that treatment with ursolic acid promotes melanosomal degradation, and bafilomycin A1 inhibition of autophagosome-lysosome fusion blocked the removal of melanosomes in α-MSH-stimulated B16F1 cells. Furthermore, depletion of the autophagy-related gene 5 (ATG5) resulted in significant suppression of ursolic acid-mediated anti-pigmentation activity and autophagy in α-MSH-treated B16F1 cells. Taken together, our results suggest that ursolic acid inhibits skin pigmentation by increasing melanosomal degradation in melanocytes.
- Subjects :
- 0301 basic medicine
ATG5
Melanoma, Experimental
Biophysics
Skin Pigmentation
Biochemistry
Melanin
Mice
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Ursolic acid
Cell Line, Tumor
Autophagy
Animals
Molecular Biology
Melanosome
Melanins
Melanosomes
integumentary system
Bafilomycin
Cell Biology
Triterpenes
Cell biology
030104 developmental biology
chemistry
alpha-MSH
030220 oncology & carcinogenesis
Intracellular
Biogenesis
Subjects
Details
- ISSN :
- 0006291X
- Volume :
- 531
- Database :
- OpenAIRE
- Journal :
- Biochemical and Biophysical Research Communications
- Accession number :
- edsair.doi.dedup.....d22fdd175e4e83d1cdf26ed3b15acc9a