Effects of the COOH-terminal tripeptide alpha-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide.
Level 5 - mechanism / opinion, no new human data
Preclinical animal (rabbit) and in vitro study
PubMed 16965771 · doi:10.1016/j.exer.2006.07.014
What was done
Rabbits underwent mechanical corneal epithelial denudation in both eyes and received topical treatment with the alpha-MSH C-terminal tripeptide KPV (1, 5, or 10 mg/ml; 30 µl, two drops four times daily for 4 days) or phosphate-buffered saline vehicle. To test nitric oxide involvement, groups received the nitric oxide donor sodium nitroprusside (SP, 10 mg/ml) or were pre-treated with the nitric oxide synthase inhibitor L-NAME (10 mg/ml) 30 minutes before KPV or SP. Corneal epithelial defect areas were measured every 12 hours via fluorescein staining and computerized image analysis. In vitro, cultured rabbit corneal epithelial cells were exposed to KPV (0.1, 1, and 10 µM) for 1, 6, and 24 hours to assess viability.
What was found
Topical KPV or SP significantly reduced the remaining epithelial defect area compared to vehicle control. At 60 hours, 8 out of 8 (100%) corneas treated with KPV or SP were completely re-epithelialized versus 0% in the vehicle group (P < 0.05). Pre-treatment with L-NAME inhibited the healing effect of KPV and completely blocked the effect of SP. In vitro, KPV at 1 and 10 µM stimulated corneal epithelial cell viability.
Why it matters
This study shows that the tripeptide KPV promotes corneal re-epithelialization in an animal model and suggests this reparative activity requires intact nitric oxide signaling.
Limits
The study is entirely preclinical, using rabbits and in vitro cell culture, which may not translate directly to humans. The abstract does not specify the total number of rabbits across all experimental arms, exact wound area measurements prior to the 60-hour mark, or long-term structural and visual outcomes.
Cited by
- supports KPV is a peptide that has been linked to angiogenesis and tissue repair.