To study the effect of SP on corneal epithelial wound healing in a mouse model of neurotrophic keratopathy, we treated eyes with a combination of FGLM-NH
2 and SSSR peptides over a 24-hour period after epithelial scraping (
Fig. 1). The possible role of NK-1R in the action of SP was examined by subconjunctival injection of the NK-1R antagonist L-733,060 24 hours before epithelial scraping and treatment onset. Immediately after corneal epithelial scraping, the size of the epithelial defect was similar in each group of mice: (1) healthy mice (6.437 ± 0.148 mm
2); (2) neurotrophic keratopathy model mice treated with PBS(–) vehicle (6.889 ± 0.550 mm
2); (3) neurotrophic keratopathy model mice treated with FGLM-NH
2 + SSSR + L-733,060 (7.700 ± 0.329 mm
2); and (4) neurotrophic keratopathy model mice treated with FGLM-NH
2 + SSSR but not L-733,060 (6.594 ± 1.034 mm
2) (
Fig. 2). Twelve hours after epithelial scraping, the epithelial defect in the FGLM-NH
2 + SSSR group (2.832 ± 1.662 mm
2) was significantly smaller than that in the PBS(–) group (5.578 ± 1.288 mm
2) of neurotrophic keratopathy model mice. At 24 hours after injury, the epithelial defect was significantly smaller in the FGLM-NH
2 + SSSR group (0.352 ± 0.443 mm
2) than in both the PBS(–) group (2.936 ± 1.342 mm
2) and the FGLM-NH
2 + SSSR + L-733,060 group (5.672 ± 1.110 mm
2) of model mice. The epithelial defect in the FGLM-NH
2 + SSSR + L-733,060 group was also significantly larger than that in the PBS(–) group. These results suggest that the FGLM-NH
2 + SSSR eyedrops promoted corneal epithelial wound healing in a manner dependent on NK-1R in mice with neurotrophic keratopathy.