Abstract
An experimental model of pressure-induced optic nerve damage promises to greatly expand understanding of the cellular events leading to retinal ganglion cell (RGC) death and of how they are influenced by intraocular pressure (IOP) and other risk factors associated with glaucoma. In this work, we propose a novel strategy employing photo-crosslinkable azidobenzoic acid-modified chitosan (Az-CH) for long-term, persistent elevation of IOP. For this purpose, a solution of Az-CH was injected into the anterior chamber of experimental rat eyes, which were subsequently irradiated with ultraviolet (UV) light to form an Az-CH gel that hindered aqueous outflow and effected prolonged IOP elevation thereby. The control eyes were treated as follows: (1) intracameral injection of Az-CH without UV irradiation, (2) intracameral injection of saline solution without UV irradiation or (3) no injection with UV irradiation. A significant IOP increase was observed in the experimental eyes, which was continuously higher for the whole testing period of 12 weeks after one-time treatment with Az-CH injection and UV irradiation. Also, a more significant loss of RGCs, one of the major features of glaucoma, was observed in experimental eyes than in the control eyes. Therefore, the strategy presented herein can be a novel experimental model to study the mechanism of RGC damage by elevated IOP over the course of a prolonged period.
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