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.

Abstract

Using a rabbit model of corneal alkali injury, this study examined whether topical H2 solution pretreatment could confer protection against subsequent oxidative damage. Eyes pretreated with H2 drops showed mild oxidative stress accompanied by upregulation of antioxidant enzymes in corneal epithelial cells. When these corneas were subsequently exposed to 0.25 M NaOH, alkali-induced oxidative stress was markedly reduced, and transparency was restored in most cases with minimal neovascularization. In contrast, buffer-pretreated corneas exhibited intense oxidative stress, scar formation, and prominent new vessel growth following alkali burn. Immunohistochemistry and pachymetry confirmed these differences. The findings indicate that H2 preconditioning elevates the intrinsic antioxidant capacity of corneal cells, thereby attenuating ROS-mediated injury and suggesting a potential role for H2 in protecting ocular tissues against various conditions involving reactive oxygen species.

Mechanism

H2 pretreatment upregulates antioxidant enzyme expression in corneal epithelial cells, enhancing ROS scavenging capacity and thereby reducing alkali-induced oxidative damage.