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Sirt3 mediates the protective effect of hydrogen in inhibiting ROS-induced retinal senescence

SIRT3 氧化应激 下调和上调 视网膜 化学 衰老 视网膜 细胞生物学 活性氧 视网膜色素上皮 DNA损伤 生物化学 生物 神经科学 DNA 锡尔图因 NAD+激酶 基因
作者
Ruichan Li,Yanli Liu,Jing Xie,Xudong Huang,Li Zhang,Hua Liu,Lihua Li
出处
期刊:Free Radical Biology and Medicine [Elsevier]
卷期号:135: 116-124 被引量:25
标识
DOI:10.1016/j.freeradbiomed.2019.02.005
摘要

Hydrogen possesses antioxidative effects and cures numerous types of ophthalmopathy, but the mechanism of hydrogen on ROS-induced retinal senescence remains elusive. In this study, retinal morphology revealed that hydrogen reduced the number and size of vitreous black deposits in Bruch's membrane in NaIO3 mice. Hydrogen also reduced ROS levels in the retina as assessed by DHE staining. Moreover, this result was consistent with the downregulation of expression of the oxidative stress hallmark OGG1. These findings suggested that hydrogen can reduce retinal oxidative stress induced by NaIO3, and this result was further verified using the antioxidant ALCAR. Mechanistic analysis revealed that hydrogen significantly inhibited the downregulation of Sirt3 expression, and this notion was confirmed using AICAR, which restores Sirt3 expression and activity. Moreover, hydrogen reduced the expression of p53, p21 and p16 and the number of blue-green precipitations in the retinas of NaIO3 mice as assessed by SA-β-gal staining. We also found that hydrogen decreased the expression of the DNA damage-related protein ATM, cyclinD1 and NF-κB but increased the expression of the DNA repair-related protein HMGB1, suggesting that hydrogen inhibits senescence in retinas of NaIO3 mice. Additionally, OCT examination revealed that hydrogen suppressed retinal high reflex formation significantly and prevented the retina from thinning. This result was supported by ERG assays that demonstrated that hydrogen prevented the reduction in a- and b-wave amplitude induced by NaIO3 in mice. Thus, our data suggest that hydrogen may inhibit retinal senescence by suppressing the downregulation of Sirt3 expression through reduced oxidative stress reactions.
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