Open AccessAcerola (Malpighia emarginata DC.) Juice Intake Suppresses UVB-Induced Skin Pigmentation in SMP30/GNL Knockout Hairless Mice
Author(s) -
Yasunori Sato,
Eriko Uchida,
Hitoshi Aoki,
Takayuki Hanamura,
Ken-ichi Nagamine,
Harubumi Kato,
Takeshi Koizumi,
Akihito Ishigami
Publication year - 2017
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0170438
Subject(s) - hairless , ascorbic acid , chemistry , transepidermal water loss , stratum corneum , melanin , food science , biochemistry , biology , genetics
Background/Aims Acerola ( Malpighia emarginata DC.) is a fruit that is known to contain high amounts of ascorbic acid (AA) and various phytochemicals. We have previously reported that AA deficiency leads to ultraviolet B (UVB)-induced skin pigmentation in senescence marker protein 30 (SMP30)/gluconolactonase (GNL) knockout (KO) hairless mice. The present study was undertaken to investigate the effects of acerola juice (AJ) intake on the skin of UVB-irradiated SMP30/GNL KO mice. Research design/Principal findings Five-week old hairless mice were given drinking water containing physiologically sufficient AA (1.5 g/L) [AA (+)], no AA [AA (-)] or 1.67% acerola juice [AJ]. All mice were exposed to UVB irradiation for 6 weeks. UVB irradiation was performed three times per week. The dorsal skin color and stratum corneum water content were measured every weekly, and finally, the AA contents of the skin was determined. The skin AA and stratum corneum water content was similar between the AA (+) and AJ groups. The L* value of the AA (+) group was significantly decreased by UVB irradiation, whereas AJ intake suppressed the decrease in the L* value throughout the experiment. Moreover, in the AJ group, there was a significant decrease in the expression level of dopachrome tautomerase, an enzyme that is involved in melanin biosynthesis. Conclusion These results indicate that AJ intake is effective in suppressing UVB-induced skin pigmentation by inhibiting melanogenesis-related genes.