目的：探讨氢对氧化应激诱导的视网膜衰老的保护机制。

方法：将小鼠随机分为三组：对照组、模型组(NaIO₃处理组)和治疗组(H₂水灌胃组)。模型组通过鼠尾静脉注射NaIO₃溶液建立视网膜氧化应激损伤模型； 对照组小鼠注射生理盐水； 治疗组予富含H₂的饮用水灌胃后造模。利用SA-β-gal染色检测视网膜衰老情况。收集小鼠视网膜，western-blot检测DNA损伤反应相关蛋白ATM、NF-κB蛋白、细胞周期蛋白D1(Cyclin D1)和DNA修复相关蛋白HMGB1的表达。

结果：SA-β-gal染色显示，治疗组蓝绿色沉淀较模型组相比减少。western-blot结果显示治疗组中DNA损伤反应相关蛋白ATM、NF-κB、Cyclin D1相对表达量(0.10±0.009、0.32±0.01、0.19±0.002)较模型组(0.77±0.08、0.70±0.02、0.36±0.01)均显著降低，差异均具有统计学意义(均P<0.01)； 而治疗组中DNA修复相关蛋白HMGB1相对表达量(0.927±0.06)较模型组(0.383±0.07)显著升高，差异有统计学意义(P<0.01)。

结论：氢可以通过抑制氧化应激诱导的DNA损伤减弱视网膜衰老。

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.