Abstract
The successful restoration of corneal innervation and function after a corneal injury is a clinically challenging issue. Structural and functional recovery after a nerve injury involves a complex series of steps in which microtubules play a key role. The aim of the current study was to investigate the effects of epothilone B (EpoB), a microtubule-stabilizing agent, on corneal innervation and the functional recovery of the corneal nerve in mice after corneal epithelial abrasion. The pretreatment of mice with EpoB has a remarkable effect on the stabilization of beta-III tubulin, as demonstrated by substantial increases in the visualization of beta-III tubulin, nerve beading, corneal reinnervation, and reaction to stimuli. Furthermore, a pharmacokinetic analysis showed that EpoB remains at a high concentration in the cornea and the trigeminal ganglion for at least 6 days after administration. In addition, the administration of EpoB at 24 hours after corneal abrasion has a marked therapeutic effect on nerve regrowth and functional recovery. In conclusion, EpoB treatment may have therapeutic utility for improving corneal reinnervation and restoring sensitivity following corneal injury.
Highlights
Located in the anterior segment of the eye, the cornea is the most important ocular medium in the visual system
Our results showed that the spinal cord and brain maintain about 10 ng of epothilone B (EpoB) per gram of tissue for more than 144 h, which is consistent with previous studies showing prolonged retention of EpoB in the CNS24
After i.p. administration, the concentration of EpoB was measured in the trigeminal ganglion, where it peaked at 122.96 ng/g at 6 h, followed by a slow elimination (Fig. 1A, Table 1)
Summary
Located in the anterior segment of the eye, the cornea is the most important ocular medium in the visual system. Recent studies have indicated that the presence of some corneal nerve tissue is important for maintaining the wetness and basal tearing of the ocular surface, as controlled by cold thermoreceptors[3]. Clinical studies have shown that corneal nerves can regenerate over a period of several years after surgical transection; the nerve density never returns to presurgical values[9]. Despite the fact that there is an urgent clinical need for the promotion of corneal nerve regeneration in neurotrophic corneas, few specific therapeutic interventions are currently available. The search for new measures to promote nerve repair is imperative
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