[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 5

A macroscopical picture of alkali-injured corneas of eyes pretreated with H₂ or buffer on days 10 and 20 after alkali injury, the central corneal thickness, and corneal neovascularization (a). Alkali-injured corneas of eyes pretreated with H₂ heal with the restoration of transparency. In contrast, the alkali-injured corneas of eyes pretreated with buffer heal with scar formation (b). The central corneal thickness (corneal hydration) is highly increased in the corneas of buffer-pretreated eyes, after only four hours following corneal alkali burn. This then decreases but did not reach the levels before injury until the end of the experiment (c). The corneal neovascularization was suppressed in the alkali-injured corneas of H₂-pretreated eyes (d). Each bar represents the from 5 corneas. The values with asterisks are significantly different () from the buffer-pretreated alkali-injured corneas. The values with asterisks are significantly different () from the buffer-pretreated alkali-injured corneas.

(a)

(b)

(c)

(d)