Trehalose treatment accelerates the healing of UVB-irradiated corneas. Comparative immunohistochemical studies on corneal cryostat sections and corneal impression cytology
Language English Country Spain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
22763875
DOI
10.14670/hh-27.1029
Knihovny.cz E-resources
- MeSH
- Urokinase-Type Plasminogen Activator metabolism MeSH
- Apoptosis drug effects MeSH
- Biomarkers metabolism MeSH
- Cytodiagnosis methods MeSH
- Radiation Injuries, Experimental drug therapy metabolism pathology MeSH
- Wound Healing drug effects MeSH
- Immunohistochemistry methods MeSH
- Injections, Intraocular MeSH
- Caspase 3 metabolism MeSH
- Rabbits MeSH
- Malondialdehyde metabolism MeSH
- Corneal Diseases drug therapy metabolism pathology MeSH
- Oxidative Stress MeSH
- Neovascularization, Pathologic drug therapy MeSH
- Epithelium, Corneal radiation effects MeSH
- Trehalose administration & dosage therapeutic use MeSH
- Tyrosine analogs & derivatives metabolism MeSH
- Ultraviolet Rays MeSH
- Frozen Sections methods MeSH
- Animals MeSH
- Check Tag
- Rabbits MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 3-nitrotyrosine MeSH Browser
- Urokinase-Type Plasminogen Activator MeSH
- Biomarkers MeSH
- Caspase 3 MeSH
- Malondialdehyde MeSH
- Trehalose MeSH
- Tyrosine MeSH
The UVB-irradiated cornea is damaged by oxidative stress. Toxic oxygen products induced by UVB radiation in the cornea are insufficiently removed by antioxidants, whose numbers decrease with increasing UVB irradiation. In addition, the UVB-irradiated cornea suffers from hypoxic conditions because damaged corneal cells cannot utilize oxygen normally, although the supply of oxygen to the cornea is unchanged (normal). This contributes to attenuated re-epithelialization, corneal neovascularization and apoptotic cell death. Our previous publications reported that trehalose applied on the corneal surface during irradiation significantly suppressed UVB-induced corneal oxidative damage. The results of this study provide for the first time important evidence that trehalose applied on the surface of corneas for two weeks following repeated UVB irradiation (312 nm, daily dose 0.5 J/cm2) accelerated corneal healing, restored corneal transparency and suppressed corneal neovascularization. Compared to buffered saline treatment, following which caspase-3, nitrotyrosine, malondialdehyde and urokinase-type plasminogen activator were still strongly expressed in the corneal epithelium two weeks after irradiation and corneal neovascularization was evident, apoptotic cell death was already significantly reduced after one week of trehalose application. The expression of other markers of injury returned to normal levels during two weeks of trehalose treatment. In conclusion, our results show that trehalose accelerated healing of the UVB irradiated cornea, very probably via suppression of hypoxia-response injury. In addition, immunohistochemical results on corneal cryostat sections corresponded with those obtained using corneal impression cytologies, thus confirming that corneal impression cytologies are useful for diagnostic purposes.
References provided by Crossref.org
The Healing of Oxidative Injuries with Trehalose in UVB-Irradiated Rabbit Corneas
