Abstract
Loliolide is a monoterpenoid hydroxylactone found in many algae, including fresh water green algae, Prasiola japonica. To date, loliolide and compounds in P. japonica have not been studied systematically with respect to skin pharmacology. In this study, we investigated oxidative stress-protective and anti-melanogenic effects of loliolide and P. japonica ethanol extract (Pj-EE), known to contain loliolide, in human keratinocyte (HaCaT) cells and mouse melanoma (B16F10) cells. Loliolide suppressed the transcription of genes encoding matrix metalloproteinases (MMPS), which were induced in HaCaT cells by hydrogen peroxide (H2O2) treatment. Loliolide and Pj-EE not only reduced the melanin secretion and content in B16F10 cells but also increased the expression of the antioxidant proteins nuclear factor (erythroid-derived 2)-like 2 (NRF2) and heme oxygenase-1 (HO-1) in HaCaT cells subjected to H2O2 treatment. Furthermore, loliolide and Pj-EE decreased expression of the anti-melanogenic protein microphthalmia-associated transcription factor (MITF) and tyrosinase in B16F10 cells subjected to α-melanocyte-stimulating hormone (α-MSH) treatment. Our findings demonstrate that loliolide and Pj-EE have antioxidant and anti-melanogenic effects on skin.
Highlights
Skin is an important organ that protects the human body from external factors and damage [1]
We evaluated the antioxidant effects of loliolide using a 2,2 -azino-bis (3-ethylbenzothiazoline6-sulphonic acid) (ABTS) assay, which can be useful to measure the level of hydroxyl radicals, with ascorbic acid as a positive control compound, since we have chosen H2O2 as an oxidative stress inducer [26]
Our study examined the antioxidant function of loliolide, a major active component found in fresh water green algae, Prasiola japonica, in keratinocyte (HaCaT) cells as well as the anti-melanogenic effects on mouse melanoma (B16F10) cells
Summary
Skin is an important organ that protects the human body from external factors and damage [1]. Since serious damage results when cells are exposed to oxidative stress, cellular antioxidants are employed as molecular defense responses. Increased expression of hemeoxygenase 1 (HO-1), which is activated by the nuclear factor (erythroid-derived 2)-like 2 (NRF2)-Kelch-like ECH-associated protein 1 (KEAP1) signaling pathway, is a defensive response [7]. NRF2-KEAP1 is inactivated by the interaction of the two proteins, but, after exposure to oxidative stress, the NRF2-KEAP1 interaction is abolished, and the separated NRF2 binds to the antioxidant response elements (AREs) of the HO-1 promoter to activate its expression. After MC1R activation, a series of intracellular signaling pathway composed of adenylyl cylase, its product, cAMP, and protein kinase A (PKA) participate in the activation of cAMP response element-binding (CREB) protein, and microphthalmia-associated transcription factor (MITF) are sequentially expressed by CREB. Synthesized MITF controls the expression of various genes such as tyrosinase, tyrosinase-related protein-1 (TRP)-1, and TRP-2 that are essential for melanin synthesis and secretion in melanocytes [9,10,11,12]
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