Enzymatically synthesized glycogen prevents ultraviolet B-induced cell damage in normal human epidermal keratinocytes

被引:6
作者
Yoshioka, Yasukiyo [1 ,2 ]
Kitakaze, Tomoya [2 ]
Mitani, Takakazu [3 ]
Furuyashiki, Takashi [4 ]
Ashida, Hitoshi [3 ]
机构
[1] Konan Womens Univ, Fac Clin Nutr & Dietet, Dept Clin Nutr & Dietet, Higashinada Ku, 6-2-23 Morikita Machi, Kobe, Hyogo 6580001, Japan
[2] Kobe Univ, Grad Sch Sci Technol & Innovat, Nada Ku, 1-1 Rokkodai Cho, Kobe, Hyogo 6518501, Japan
[3] Kobe Univ, Grad Sch Agr Sci, Dept Agrobiosci, Nada Ku, 1-1 Rokkodai Cho, Kobe, Hyogo 6518501, Japan
[4] Ezaki Glico Co Ltd, Inst Hlth Sci, Nishiyodogawa Ku, 4-6-5 Utajima, Osaka 5558502, Japan
关键词
enzymatically synthesized glycogen; ultraviolet B; reactive oxygen species; anti-oxidative protein; normal human epidermal keratinocytes; TRANSCRIPTION FACTOR NRF2; MOLECULAR-MECHANISMS; OXIDATIVE STRESS; ACTIVATION; ANTIOXIDANT; PROTECTS; RADIATION; SUPPRESSION; BINDING; ALPHA;
D O I
10.3164/jcbn.20-44
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Enzymatically synthesized glycogen is a product from starch. Enzymatically synthesized glycogen has been reported to possess various health beneficial effects such as anti-oxidative and anti-inflammatory effects. In this study, we investigated the effect of enzymatically synthesized glycogen on ultraviolet B-induced oxidative stress and apoptosis in normal human epidermal keratinocytes. Treatment with enzymatically synthesized glycogen suppressed ultraviolet B-induced reactive oxygen species, caspase-3 activity, and DNA fragmentation in normal human epidermal keratinocytes. Furthermore, enzymatically synthesized glycogen increased in the expression level of heme oxygenase-1, NAD(P)H: quinone oxidoreductase 1, and NF-E2-related factor 2, a transcriptional factor for heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1. Although enzymatically synthesized glycogen did not increase in its mRNA expression level of NF-E2-related factor 2, enzymatically synthesized glycogen retained its protein degradation. Knockdown of heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 canceled enzymatically synthesized glycogen-suppressed reactive oxygen species accumulation in normal human epidermal keratinocytes. It is, therefore, concluded that enzymatically synthesized glycogen inhibited ultraviolet B-induced oxidative stress through increasing the expression level of heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 through the NF-E2-related factor 2 pathway in normal human epidermal keratinocytes.
引用
收藏
页码:36 / 42
页数:7
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