Skin damage induced by zinc oxide nanoparticles combined with UVB is mediated by activating cell pyroptosis via the NLRP3 inflammasome-autophagy-exosomal pathway

CNU IR > Pharmacy and Science > Dept. of Cosmetic Science and institute of cosmetic science > Other Projects > Item 310902800/34675

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://ir.cnu.edu.tw/handle/310902800/34675

题名:	Skin damage induced by zinc oxide nanoparticles combined with UVB is mediated by activating cell pyroptosis via the NLRP3 inflammasome-autophagy-exosomal pathway
作者:	Chen, Yu-Ying Lee, Yu-Hsuan Wang, Bour-, Jr. Chen, Rong-Jane Wang, Ying-Jan
贡献者:	National Cheng Kung University China Medical University Taiwan Department of Cosmetic Science and Institute of Cosmetic Science, Chia Nan University of Pharmacy & Science National Cheng Kung University National Cheng Kung University Hospital National Cheng Kung University China Medical University Taiwan China Medical University Hospital - Taiwan
关键词:	antibacterial activity titanium-dioxide in-vitro penetration size pterostilbene cytotoxicity dysfunction inhibition toxicity
日期:	2022
上传时间:	2023-12-11 14:04:35 (UTC+8)
出版者:	BMC
摘要:	Background Zinc oxide nanoparticles (ZnONPs) are widely used nanomaterial in personal cosmetics, such as skin creams and sunscreens, due to their whitening properties and strong UV light absorption. However, the safety issues and the hazards of ZnONPs, which can be taken up by the skin and cause skin toxicity, are still unclear. From a chemoprevention point of view, pterostilbene (PT) has been reported to prevent skin damage effectively by its anti-inflammatory and autophagy inducer effect. This study aims to determine the skin toxicity and the potential mechanisms of UVB and ZnONPs exposure and the preventive effect of PT. Results The co-exposure of UVB and ZnONPs elicit NLRP3 inflammasome activation and pyroptosis in keratinocytes. Furthermore, exposure to both UVB and ZnONPs also disrupts cellular autophagy, which increases cell exosome release. In vivo UVB and ZnONPs exposure triggers skin toxicity, as indicated by increased histological injury, skin thickness and transepidermal water loss. Notably, the NLRP3 inflammasome-mediated pyroptosis are also activated during exposure. Topical application of pterostilbene attenuates NLRP3 inflammasome activation and pyroptosis by decreasing ROS generation and mitochondrial ROS (mtROS) levels. In addition to its antioxidant effect, PT also reversed autophagy abnormalities by restoring normal autophagic flux and decreasing NLRP3 inflammasome-loaded exosome release. Conclusions Our findings reveal that ZnONPs induce skin damage in conjunction with UVB exposure. This process involves an interplay of inflammasomes, pyroptosis, autophagy dysfunction, and exosomes in skin toxicity. PT alleviates skin inflammation by regulating the inflammasome-autophagy-exosome pathway, a finding which could prove valuable when further evaluating ZnONPs effects for cosmetic applications.
關聯:	PARTICLE AND FIBRE TOXICOLOGY, v.19, Article number: 2
显示于类别:	[Dept. of Cosmetic Science and institute of cosmetic science] Other Projects

文件中的档案:

档案	描述	大小	格式	浏览次数
index.html		0Kb	HTML	549	检视/开启
s12989-021-00443-w.pdf		9907Kb	Adobe PDF	172	检视/开启

在CNU IR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....