Background: The ability to scavenge reactive oxygen species (ROS) is crucial for cornea epithelial cells to resist oxidative damage. The authors previously demonstrated that exogenous thymosin beta-4 (Tβ4) was able to protect human cornea epithelial (HCE-T) cells against H 202-induced oxidative damage, and its cellular inter-nalisation was essential. The aim of this study is to further elucidate its protective mechanism. Methods: HCE-T cells with or without Tβ4 pretreatment were exposed to H202, and the differences in caspase activity, intracellular ROS levels, cell viability, and the expression of anti-oxidative enzymes, were measured and compared. Results: Besides reducing caspase-9 activation and intracellular ROS levels induced by H202, treatment of Tβ4 could also increase cell viability and stimulate the expression of manganese superoxide dismutase (SOD) and copper/zinc SOD. Moreover, both transcription and translation levels of catalase were also upregulated by Tβ4 in the presence of exogenous H202. Furthermore, it was demonstrated that the addition of catalase inhibitor abrogated the protective effect of Tβ4 against H202-induced oxidative damage. Conclusion: To the best of the authors' knowledge, this is the first report to show that Tβ4 was capable of upregulating anti-oxidative enzymes in human corneal epithelial cells, and these findings further support its role in cornea protection.
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