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Air pollutant particulate matter 2.5 induces dry eye syndrome in mice
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Air pollutant particulate matter 2.5 induces dry eye syndrome in mice
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Journal Article
Air pollutant particulate matter 2.5 induces dry eye syndrome in mice
2018
Overview
In this study, we explored the effects of particulate matter 2.5 (PM
2
.
5
) eye drops on the ocular surface structure and tear function in mice and established a novel animal model for dry eye research. We found that, following treatment with PM
2.5
, the tear volume and, the tear film break-up time showed statistical differences at each time point (P < 0.05). The FL score of the PM
2.5
-treated group was higher than that of others (P < 0.05). The average number of corneal epithelial layer cells in groups A and B was significantly lower than that in group C (P < 0.05). Scanning electron microscopy and transmission electron microscopy revealed that the number of corneal epithelial microvilli and corneal desmosomes was drastically reduced in group C. PM
2.5
induced apoptosis in the corneal superficial and basal epithelium and led to abnormal differentiation and proliferation of the ocular surface with higher expression levels of Ki67 and a reduced number of goblet cells in the conjunctival fornix in group C. PM
2.5
significantly increased the levels of TNF-α, NF-κB p65 (phospho S536), and NF-κB in the cornea. Thus, the topical administration of PM
2.5
in mice induces ocular surface changes that are similar to those of dry eye in humans, representing a novel model of dry eye.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 14/63
/ 64/60
/ 82/1
/ 96/2
/ Animals
/ Cell Proliferation - drug effects
/ Cornea
/ Dry Eye Syndromes - chemically induced
/ Dry Eye Syndromes - metabolism
/ Dry Eye Syndromes - pathology
/ Epithelium, Corneal - metabolism
/ Epithelium, Corneal - ultrastructure
/ Eye
/ Fornix
/ Gene Expression Regulation - drug effects
/ Humanities and Social Sciences
/ Humans
/ Mice
/ Particulate Matter - toxicity
/ Scanning electron microscopy
/ Science
/ Structure-function relationships
