Enzymatically synthesized glycogen protects inflammation induced by urban particulate matter in normal human epidermal keratinocytes

Enzymatically synthesized glycogen protects inflammation induced by urban particulate matter in normal human epidermal keratinocytes
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DOI:
10.3164/jcbn.20-43
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发表时间:
2020-06
影响因子:
2.4
通讯作者:
T. Kitakaze;Yasukiyo Yoshioka;T. Furuyashiki;H. Ashida
T. Kitakaze;Yasukiyo Yoshioka;T. Furuyashiki;H. Ashida
中科院分区:
医学4区
文献类型:
--
作者:
T. Kitakaze;Yasukiyo Yoshioka;T. Furuyashiki;H. Ashida

文献摘要

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城市颗粒物(PM)暴露与外源性皮肤老化迹象和皮肤癌发病率显著相关。PM含有多环芳烃,它们是芳烃受体(AhR)的激动剂。AhR的激活促进细胞内活性氧(ROS)的产生和炎症。酶合成糖原(ESG)是一种由淀粉合成的糖原,具有抗肿瘤、抗肥胖、抗氧化等多种功能。然而,ESG对pm诱导的皮肤炎症的影响尚不清楚。在这项研究中,我们研究了ESG是否对pm诱导的人表皮角质形成细胞的氧化应激和炎症有保护作用。ESG抑制pm诱导的炎症因子IL6、TNFA和PTGS2的表达。ESG还抑制pm诱导的MAPKs磷酸化和ROS积累。然而,ESG对pm诱导的AhR靶蛋白之一CYP1A1的表达没有影响。另一方面,ESG增加了Nrf2的核易位和抗氧化蛋白HO-1和NQO1的表达。这些结果表明,ESG通过Nrf2途径减少ROS积累,从而抑制pm诱导的炎症。
Urban particulate matters (PM) exposure is significantly correlated with extrinsic skin aging signs and skin cancer incidence. PM contains polycyclic aromatic hydrocarbons, and they act as the agonists of aryl hydrocarbon receptor (AhR). Activation of AhR promotes generation of intracellular reactive oxygen species (ROS) and inflammation. Enzymatically synthesized glycogen (ESG), which is synthesized from starch, possesses various functions, such as anti-tumor, anti-obesity and antioxidant. However, the effects of ESG on PM-induced skin inflammation remain unclear. In this study, we investigated whether ESG has a protective effect on PM-induced oxidative stress and inflammation in human epidermal keratinocytes. ESG inhibited PM-induced expression of inflammatory cytokines IL6, TNFA and PTGS2. ESG also inhibited PM-induced phosphorylation of MAPKs and ROS accumulation. However, ESG had no effect on PM-induced expression of CYP1A1, one of the target proteins of AhR. On the other hand, ESG increased nuclear translocation of Nrf2 and expression of antioxidant proteins, HO-1 and NQO1. These results suggest that ESG suppressed PM-induced inflammation by decreasing ROS accumulation through the Nrf2 pathway.