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Fig. 3 | Particle and Fibre Toxicology

Fig. 3

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. 3

ZnONP- and UVB-induced Mitochondrial damage and NLRP3 inflammasome activation in HaCaT cells. A Mitotracker Deep Red was employed to examine ZnONP-induced mitochondrial membrane potential (MMP) loss via flow cytometry after 24 h exposure. B Histograms represent the percentage of MMP loss. C mtROS generation were examined by flow cytometry in HaCaT cells after ZnONPs and UVB treatment in 3 h. D Histograms represent the fluorescence intensity of mtROS. E ROS generation were examined by flow cytometry in HaCaT cells after ZnONPs and UVB treatment in 3 h. F Histograms represent the fluorescence intensity of ROS. G, H Western blot analysis of the levels of the NLRP3 inflammasome proteins NLRP3, ASC, pro-caspase-1 and cleaved caspase-1 in HaCaT cells. GAPDH was used as a loading control. I LDH release in ZnONP-treated HaCaT cells. Values are presented as the mean ± SD (n = 3). *p < 0.05, control group versus treatment groups. #p < 0.05, the UVB + ZnONPs groups versus the UVB + ZnONPs + PT groups

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