Molecular Hydrogen Effectively Heals Alkali-Injured Cornea via Suppression of Oxidative Stress

• Published in: Oxidative medicine and cellular longevity 2017-01, Vol.2017 (2017), p.1-12
• Main Authors: Holan, Vladimir, Hermankova, Barbora, Kossl, Jan, Cejka, Cestmir, Cejkova, Jitka
• Format: Article
• Language: English
• Subjects: Actins - metabolism; Animals; Antioxidants; Burns; Cornea - metabolism; Cornea - pathology; Corneal Injuries - etiology; Corneal Injuries - metabolism; Corneal Injuries - pathology; Cytokines; Cytokines - metabolism; Disease Models, Animal; Enzymes; Female; Gene Expression - drug effects; Growth factors; Hydrogen; Hydrogen - pharmacology; Immunohistochemistry; Interleukin-1beta - genetics; Interleukin-1beta - metabolism; Irrigation; Keratin-12 - metabolism; Keratin-3 - metabolism; Malondialdehyde - metabolism; Nitric oxide; Oxidative stress; Oxidative Stress - drug effects; Peroxynitrous Acid - metabolism; Physiological aspects; Physiology; Rabbits; Rodents; Sodium Hydroxide - toxicity; Studies; Vascular Endothelial Growth Factor A - genetics; Vascular Endothelial Growth Factor A - metabolism
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2017/8906027

The aim of this study was to examine the effect of molecular hydrogen (H2) on the healing of alkali-injured cornea. The effects of the solution of H2 in phosphate buffered saline (PBS) or PBS alone topically applied on the alkali-injured rabbit cornea with 0.25 M NaOH were investigated using immunohistochemical and biochemical methods. Central corneal thickness taken as an index of corneal hydration was measured with an ultrasonic pachymeter. Results show that irrigation of the damaged eyes with H2 solution immediately after the injury and then within next five days renewed corneal transparency lost after the injury and reduced corneal hydration increased after the injury to physiological levels within ten days after the injury. In contrast, in injured corneas treated with PBS, the transparency of damaged corneas remained lost and corneal hydration elevated. Later results—on day 20 after the injury—showed that in alkali-injured corneas treated with H2 solution the expression of proinflammatory cytokines, peroxynitrite, detected by nitrotyrosine residues (NT), and malondialdehyde (MDA) expressions were very low or absent compared to PBS treated injured corneas, where NT and MDA expressions were present. In conclusion, H2 solution favorably influenced corneal healing after alkali injury via suppression of oxidative stress.