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Fig. 4 | Particle and Fibre Toxicology

Fig. 4

From: Acute and continuous exposure of airborne fine particulate matter (PM2.5): diverse outer blood–retinal barrier damages and disease susceptibilities

Fig. 4

Continuous PM2.5 exposure prompts irregular repair of RPE barrier structure in mice. A Expression of inflammation-related proteins in mouse RPE/choroidal tissues under exposure of PBS or PM2.5 for 3 weeks suggested by immunoblotting. GAPDH served as the internal control. PBS, phosphate buffer saline; RPE, retinal pigment epithelium; IL1B, interleukin 1 beta; IL6, interleukin 6; TNF-α, tumor necrosis factor; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. B Quantification of shown blots, normalized by GAPDH (n = 3). C, D Immunofluorescence staining of RPE65 and ZO1 on RPE flat-mounts in mice treated with PBS or PM2.5 for 3 weeks. E Expression of RPE65 and TJ protein Occludin in mouse RPE/choroidal tissues suggested by immunoblotting. GAPDH served as the internal control. F Quantification of shown blot, normalized by GAPDH (n = 3). G Hydration rate of retina in mice treated with PBS or PM2.5 for 3 weeks (n = 8). Data in (B, F, G) are presented as mean ± SD. *p < 0.05, and **p < 0.01

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