Enzymatically synthesized glycogen prevents ultraviolet B-induced cell damage in normal human epidermal keratinocytes
Enzymatically synthesized glycogen prevents ultraviolet B-induced cell damage in normal human epidermal keratinocytes
复制标题
DOI：
10.3164/jcbn.20-44
复制
发表时间：
2020-06
影响因子：
2.4
通讯作者：
Yasukiyo Yoshioka;T. Kitakaze;Takakazu Mitani;T. Furuyashiki;H. Ashida
中科院分区：
文献类型：
--
作者：
Yasukiyo Yoshioka;T. Kitakaze;Takakazu Mitani;T. Furuyashiki;H. Ashida
酶促合成的糖原是淀粉的产物。据报道，酶促合成的糖原具有多种有益健康的作用，如抗氧化和抗炎作用。在这项研究中，我们研究了酶促合成的糖原对中波紫外线诱导的氧化应激和正常人表皮角质形成细胞凋亡的影响。用酶促合成的糖原治疗抑制了正常人表皮角质形成细胞中紫外线B诱导的活性氧、半胱天冬酶-3活性和DNA片段化。此外，酶促合成的糖原增加了血红素加氧酶-1、NAD（P）H：醌氧化还原酶1和NF-E2相关因子2（血红素加氧酶-1和NAD（P）H：醌氧化还原酶1的转录因子）的表达水平。虽然酶促合成的糖原没有增加其NF-E2相关因子2的mRNA表达水平，酶促合成的糖原保留其蛋白质降解。血红素加氧酶-1和NAD（P）H：醌氧化还原酶1的敲低取消了正常人表皮角质形成细胞中酶促合成糖原抑制的活性氧簇积累。因此，可以得出结论，在正常人表皮角质形成细胞中，酶促合成的糖原通过NF-E2相关因子2途径增加血红素加氧酶-1和NAD（P）H：醌氧化还原酶1的表达水平来抑制UVB诱导的氧化应激。
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.