Corneal Endothelial Dysfunction Introduction

Due to the limited regenerative capacity of the corneal endothelium in vivo, massive cell loss due to injury, toxic injury, or disease can quickly exceed the functional reserve of the corneal endothelium and lead to irreversible endothelial dysfunction, clinically manifested as corneal edema, bullous keratopathy, and vision loss. Keratoplasty has long been considered the gold standard for severe corneal edema. Despite the relatively high success rate of keratoplasty, there is still an urgent global clinical need to identify improved therapeutic strategies to address this condition. There is a growing need for preclinical animal models of corneal endothelial dysfunction to assess the safety and efficacy of novel therapies. Rabbits offer significant advantages for this type of research, such as large eyes, relatively low cost, and ethical considerations. They are most commonly used for in vivo CEC therapy studies.

Fig. 1. Effects of benzalkonium chloride on rabbit corneal endothelial cell morphology. (Zhang Z, et al., 2014)

Service Overview

Benzalkonium chloride (BAC) is one of the most commonly used preservatives in ophthalmic preparations, and when it is introduced into the anterior chamber, it can cause corneal endothelial cell (CEC) toxicity. It is widely used as a drug to induce corneal endothelial damage in experimental animals. Ace Therapeutics find that a population of corneal endothelial progenitor cells reside in the transition zone between the peripheral cornea and the trabecular meshwork, suggesting that chemical injury induced by intracameral injection leads to more extensive CEC injury. In view of this, our researchers develop a stable and reproducible BAC-induced corneal endothelial injury model by exploring the injury of corneal endothelial cells by anterior chamber injection of chemical substances like BAC.

Explore Ace Therapeutics' Rabbit Model of Benzalkonium Chloride-Induced Corneal Endothelial Injury

Ace Therapeutics' corneal endothelial injury model was induced by injecting 0.05% benzalkonium chloride into the anterior chamber of adult New Zealand white rabbits. The follow-up period was up to 14 days.

Model characteristics: Corneal edema, increased central corneal thickness, disrupted corneal endothelial cell morphology, and increased mortality.

Available Support Services

In order to comprehensively assess corneal endothelial damage, such as morphology and mortality of corneal endothelial cells, our researchers performed a full range of measurements, including but not limited to:

• Ophthalmology examination.
• Corneal pachymetry.
• Vital staining and histological evaluation.
• Confocal microscopy (IVCM).
• Molecular biology analysis (ELISA, WB, qPCR).

In addition, our researchers also chose the clinically relevant compound to fully implement and validate the model's reliability.

Ace Therapeutics aims to provide customers worldwide with a novel and relatively easy-to-perform procedure for testing new therapeutic strategies for restoring the corneal endothelium. If you are interested in our services or need more detailed information, please feel free to contact us. Our experienced scientists are ready to help you!

References

1. Park S, Leonard BC, Raghunathan VK, et al. Animal models of corneal endothelial dysfunction to facilitate development of novel therapies. Ann Transl Med. 2021, 9(15):1271.
2. Zhang Z, Huang Y, Xie H, et al. Benzalkonium chloride suppresses rabbit corneal endothelium intercellular gap junction communication. PLoS One. 2014, 9(10):e109708.
3. Sergi S, Marta L, Daniel C, et al. A Rabbit Model of Corneal Endothelial Injury Induced by Intracameral Injection of 0.05% Benzalkonium Chloride. International Journal of Ophthalmic Research. 2020, 6(1):344-351.

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