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Fig. 9 | Particle and Fibre Toxicology

Fig. 9

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

Fig. 9

Schematic of the mechanism by which ZnONPs and UVB induce dermal toxicity and the inhibition mechanism of PT. Exposure to ZnONPs and UVB induced NLRP3 inflammasome-related pyroptosis, autophagy dysfunction and NLRP3 inflammasome loaded exosome secretion in keratinocytes. ZnONPs and UVB induced NLRP3 inflammasome, and pyroptosis through ROS generation and mitochondrial dysfunction. Moreover, ZnONPs also caused cell autophagy dysfunction (red cross), inhibited the fusion of NLPR3 complex protein loaded MVB and autophagosomes to form amphisome, which thereby inhibited the degradation of cargo in MVB and increased the amount of exosome-containing NLRP3 complex that propagated. In addition, PT protected HaCaT cells by attenuating ZnONP- and UVB-induced ROS generation and autophagy dysfunction

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Particle and Fibre Toxicology

ISSN: 1743-8977

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