AIM: To investigate the protective mechanism of hydrogen on retinal senescence induced by oxidative stress.

METHODS: Mice were randomly divided into three groups: control group, model group and treatment group. Animal models of retinal oxidative stress injury were established by injecting sodium iodate solution into mice caudal vein. Harvesting the mice retina, Western-blot was used to detect the level of proteins related to DNA damage response such as ATM, NF-κB, cyclin D1 and HMGB1 that associated with DNA repair.

RESULTS: SA-β-gal staining showed that the blue-green deposits in treatment group were reduced than that in model group. The expression of DNA damage reactive protein in treatment group ATM, cyclin D1, NF-κB(0.10±0.009, 0.32±0.01, 0.19±0.002)were significantly lower than those in the model groups(0.77±0.08, 0.70±0.02, 0.36±0.01), and the differences were statistically significant(all P<0.01). At the same time, the expression of DNA repair protein HMGB1 in treatment group(0.927±0.06)were notably higher than that in model group(0.383±0.07)and the difference was statistically significant(P<0.01).

CONCLUSION: H₂ can attenuate senescence by inhibiting oxidative-stress induced DNA damage.