Research Article
[Retracted] An Immunohistochemical Study of the Increase in Antioxidant Capacity of Corneal Epithelial Cells by Molecular Hydrogen, Leading to the Suppression of Alkali-Induced Oxidative Stress
Figure 3
In alkali-injured corneal epithelium of H2-pretreated eyes, the alkali-induced oxidative stress is suppressed. The animals were euthanized immediately after corneal alkali injury, followed after three-day pretreatment of healthy eyes with H2 or buffer and the corneas examined. Compared to the alkali-injured corneas of buffer-pretreated eyes, where oxidative stress is strong in the corneal epithelium and expressions of antioxidant enzymes (SOD, CAT) decreased, in the alkali-injured corneal epithelium of H2-pretreated eyes, the oxidative stress is reduced and the expression of antioxidant enzymes is nearly at physiological levels (compared to controls). DHE, SOD, and CAT expression intensities are quantified. The values with asterisks are significantly different (, , ) from the buffer-pretreated corneas. Buffer-pretreated DHE ; H2-pretreated DHE ; control DHE ; buffer-pretreated SOD ; H2-pretreated SOD ; control SOD ; buffer-pretreated CAT ; H2-pretreated CAT ; control CAT ; /group. Scale bars: 50 μm.