Thymosin beta-4 upregulates anti-oxidative enzymes and protects human cornea epithelial cells against oxidative damage.

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 (Tβ 4 ) was able to protect human cornea epithelial (HCE-T) cells against H 2 O 2 -induced oxidative damage, and its cellular internalisation was essential. The aim of this study is to further elucidate its protective mechanism. Methods: HCE-T cells with or without Tβ 4 pretreatment were exposed to H 2 O 2 , 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 H 2 O 2 , treatment of Tβ 4 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 Tβ 4 in the presence of exogenous H 2 O 2 . Furthermore, it was demonstrated that the addition of catalase inhibitor abrogated the protective effect of Tβ 4 against H 2 O 2 -induced oxidative damage. Conclusion: To the best of the authors9 knowledge, this is the first report to show that Tβ 4 was capable of upregulating anti-oxidative enzymes in human corneal epithelial cells, and these findings further support its role in cornea protection.