The size-dependence and reversibility of polystyrene nanoplastics-induced hepatic pyroptosis in mice through TXNIP/NLRP3/GSDMD pathway

被引:0
作者
Lu, Yan-Yang [1 ]
Hua, Weizhen [1 ]
Lu, Lu [1 ]
Tian, Meiping [1 ]
Huang, Qingyu [1 ]
机构
[1] Chinese Acad Sci, Inst Urban Environm, Key Lab Urban Environm & Hlth, Xiamen 361021, Peoples R China
基金
中国国家自然科学基金;
关键词
nanoplastics; pyroptosis; hepatotoxicity; TXNIP; NLRP3; HEPATOCYTE PYROPTOSIS; INFLAMMASOME; ACTIVATION;
D O I
10.1093/toxres/tfae106
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
As emerging environmental contaminants, nanoplastics (NPs) are progressively accumulating in terrestrial and aquatic ecosystems worldwide, posing a potential threat to human health. The liver is considered as one of the primary organs targeted by NPs accumulation in living organisms. However, there remains a large knowledge gap concerning NPs-induced hepatotoxicity. In this study, we examined the impact of chronic exposure to environmentally relevant doses of polystyrene (PS) NPs on hepatic pyroptosis in mice. The results demonstrated that both particle sizes of PS-NPs (100 nm and 500 nm) significantly triggered pyroptosis in the mouse liver, as evidenced by the upregulation of GSDMD-N protein levels; moreover, this pyroptotic effect induced by 100 nm PS-NPs was more pronounced compared to that of 500 nm PS-NPs. Mechanistically, exposure to 100 nm and 500 nm PS-NPs resulted in an upregulation of TXNIP protein expression, thereby activating NLRP3 inflammasome and subsequently inducing inflammatory responses and pyroptosis. Notably, following the termination of PS-NPs exposure and a subsequent recovery period of 50 days, PS-NPs-mediated inflammation and pyroptosis via TXNIP/NLRP3 pathway were effectively ameliorated, even returning to levels close to the baseline. Collectively, our findings provide novel evidence for the size-dependence and reversibility of NPs-induced hepatic pyroptosis through TXNIP/NLRP3/GSDMD pathway in vivo. Graphical Abstract
引用
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页数:9
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