| Purpose: To establish a convenient murine model of dry eye induced by osmotic dehydration.Methods: Corneal epithelial erosion was induced by exposure of 4- to 6-week-old BALB/c mice eyes to a sugar powder for 12 hours, which provokes the rapid removal of corneal surface liquid. The resultant changes in corneal barrier function by means of corneal fluorescein staining (score, 0–15), corneal scanning electron microscopy, and histopathologic examination of cornea were then analyzed. The apoptosis in the epithelium was determined by immunohistochemical assay for active caspase-3.
Results: The mice corneas exposed to continuous hyperosmotic stress showed a increased corneal fluorescein staining, marked thickening and accelerated desquamation of the apical corneal epithelium cells compared with baseline. Active caspase-3 was highly expressed in the corneal epithelia after 12 hours of hyperosmotic treatment.
Conclusion: These results demonstrated that the present murine in vivo model may be used to conveniently screen therapeutics against acute ocular diseases with corneal epithelium damage. In addition, apoptotic cell death may be at least partially responsible for the hyperosmolarity-induced destruction of the corneal epithelium.
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