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Updated: Sep 23, 2026
Establishment of A Mouse Model of Aqueous Deficiency Dry Eye
Published on: November 1, 2024
A convenient rabbit model of ocular epithelium damage induced by osmotic dehydration
Iwao Katsuyama1, Tsutomu Arakawa
1Biochemical and Pharmacological Laboratories Inc., Osaka, Japan. i.katsuyama@bpl.co.jp
Abstract:
Dry eye is an ocular disease clinically associated with corneal epithelium damage and arises acutely or chronically from dehydration of the ocular surface. We provide herein a novel in vivo model of corneal epithelium damage, in which the corneal surface was entirely covered with a sugar powder to provoke the rapid removal of corneal surface liquid. In this animal model, such corneal damage as can be fluorometrically detected was observed immediately after 20-minute hyperosmotic treatment, reached a maximum 6 hours later, and then gradually declined to complete recovery at Hour 126. Recovery of the damaged corneas produced by hyperosmotic stress was significantly accelerated by treatment with 0.1% sodium hyaluronate, a dry eye remedy in Japan. Thinning or partial erosion of the epithelial cell layers was histopathologically demonstrated in and around the sugar powder-applied area but the posterior stromal cell layer remained intact, indicating that the present rabbit in vivo model may be used to conveniently screen therapeutics against acute ocular diseases with corneal epithelium damage. In addition, microscopic observations of TUNEL-stained thin-sections of the damaged corneas indicated that apoptotic cell death, but not any inflammatory reactions, may be at least partially responsible for the hyperosmolarity-induced destruction of the corneal epithelium.
Insights
Researchers developed a novel rabbit model for corneal epithelium damage using hyperosmotic sugar powder treatment. This model effectively simulates dry eye conditions and shows accelerated healing with sodium hyaluronate treatment.
Area of Science:
- Ophthalmology
- Cell Biology
- Drug Discovery
Background:
- Dry eye disease is characterized by corneal epithelium damage due to ocular surface dehydration.
- Existing models may not fully capture acute or chronic dry eye conditions.
- Novel in vivo models are needed for effective therapeutic screening.
Purpose of the Study:
- To establish a novel rabbit in vivo model for acute corneal epithelium damage.
- To investigate the mechanism of hyperosmolarity-induced corneal damage.
- To evaluate the therapeutic potential of sodium hyaluronate in this model.
Main Methods:
- Corneal epithelium damage induced by covering the ocular surface with sugar powder for 20 minutes.
- Damage assessment using fluorometry and histopathology.
- TUNEL staining to evaluate apoptotic cell death.
- Treatment with 0.1% sodium hyaluronate to assess therapeutic efficacy.
Main Results:
- Immediate corneal damage detected post-treatment, peaking at 6 hours, with full recovery by 126 hours.
- Histopathology confirmed epithelial thinning and erosion, with intact stromal layers.
- Sodium hyaluronate significantly accelerated corneal recovery.
- TUNEL staining indicated apoptotic cell death as a key mechanism, with no significant inflammatory response.
Conclusions:
- The developed rabbit model provides a convenient platform for screening therapeutics against acute ocular surface diseases.
- Hyperosmolarity induces corneal epithelium damage primarily through apoptosis.
- 0.1% sodium hyaluronate demonstrates therapeutic efficacy in accelerating recovery from this induced damage.
