氢对氧化应激诱导的视网膜衰老的保护机制

Protective mechanism of hydrogen on oxidative stress-induced retinal aging

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。

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.