The Ethanol Extract of Musa sapientum Linn. Peel Inhibits Melanogenesis through AKT Signaling Pathway

Hyperpigmentation caused by melanin overproduction can be induced by UV radiation. The quest for effective depigmenting agents continues because many anti-melanin agents have restricted use and/or produce side-effects. The present study was aimed to investigate the inhibitory activity of Musa sapien...

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Bibliographic Details
Published in:Cosmetics (Basel) 2021-09, Vol.8 (3), p.70
Main Authors: Phacharapiyangkul, Naphichaya, Thirapanmethee, Krit, Sa-ngiamsuntorn, Khanit, Panich, Uraiwan, Lee, Che-Hsin, Chomnawang, Mullika Traidej
Format: Article
Language:English
Subjects:
Acids
AKT protein
Antibodies
Autophagy
banana
Bananas
cell signaling pathway
Enzymes
Ethanol
Hyperpigmentation
Kinases
Melanin
melanogenesis
Melanoma
Microphthalmia-associated transcription factor
Microtubule-associated protein 1
Musa sapientum
Penicillin
Phagocytosis
phenolic compounds
Phosphorylation
Proteins
Signal transduction
Ultraviolet radiation
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Summary:Hyperpigmentation caused by melanin overproduction can be induced by UV radiation. The quest for effective depigmenting agents continues because many anti-melanin agents have restricted use and/or produce side-effects. The present study was aimed to investigate the inhibitory activity of Musa sapientum Linn. (AA group) peel ethanol extracts (MPE) on α-melanocyte stimulating hormone (α-MSH)-induced melanin production. In addition, the molecular mechanism related to this process was examined in B16F10 mouse melanoma cells. The results indicated that MPE remarkably inhibited melanogenesis in α-MSH-stimulated B16F10 cells. Microphthalmia-associated transcription factor (MITF) and tyrosinase expressions were suppressed by MPE in a concentration-dependent manner. In addition, MPE significantly decreased the expression of melanosome transfer protein markers (Rab27a and Pmel17) in a dose-dependent manner. This study found that the elevated phosphorylation of AKT in the B16F10 cells was diminished by MPE treatment. Furthermore, microtubule-associated protein 1 light chain 3 (LC3)-II and p62 (autophagy markers) were affected after the B16F10 cells were treated with MPE. This study demonstrated that MPE might be an effective agent for anti-melanogenesis through the AKT pathway, subsequently diminishing MITF expression and tyrosinase enzyme family production. The findings indicated that MPE could potentially serve as a depigmenting agent in cosmeceuticals.
ISSN:2079-9284
2079-9284
DOI:10.3390/cosmetics8030070