Fig. 2

Long-term chronic exposure to PM2.5 breaks corneal homeostasis of rats. (A) A long-term PM2.5-exposed rat model was established, and ocular surface health was monitored by ophthalmological (slit lamp examination and Schirmer’s test), pathological (H&E staining), and molecular biological technologies (immunofluorescence staining). (B) Rat body weights of the PM2.5 or PBS group in 3 weeks. N = 5 in each group. (C) Slit lamp examination was used to examine corneal epithelium defect and results showed more corneal staining of fluorescein sodium occurred under cobalt-blue light in the PM2.5 treatment group. The red arrows pointed to the corneal epithelium defect. N = 5 in each group. (D) Schirmer’s test indicated that prolonged PM2.5 exposure caused more severe damage in tear secretion in the PM2.5 group. N = 5 in each group. *p < 0.05, ** p < 0.01 compared with indicated group, #p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001 compared with the results of their own group at 0 days. (E) Anatomical structures of the cornea. (F) H&E staining showed structural changes between the two groups (scale bar, 100 μm). The cornea epithelium thickness of the PM2.5 group got thinner. N = 5 in each group. ***p < 0.001. (G) Immunofluorescence staining showed the expression of proliferation marker Ki67 significantly decreased on rat cornea in the PM2.5 group (scale bar, 100 μm). N = 3 in each group. The white arrowhead indicated Ki67⁺ cells. *p < 0.05. (H) Immunofluorescence staining showed the expression of tight junction marker ZO-1 decreased on rat cornea in the PM2.5 group (scale bar, 100 μm). N = 3 in each group. ****p < 0.0001. PBS: the PBS eyedrop administration group; PM: the PM2.5 eyedrop administration group