Hydrogen sulfide protects retina from blue light-induced photodamage and degeneration via inhibiting ROS-mediated ER stress-CHOP apoptosis signal

IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Sen Zhu, Xuan Li, B. Dang, Fen-Shiun Wu, K. Gou, Chunming Wang, Changjun Lin
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引用次数: 9

Abstract

ABSTRACT Background: Hydrogen sulfide (H2S) is a small reducing gas molecule with various biological functions such as anti-oxidative, anti-apoptotic and anti-inflammatory activities. In this study, we investigated the therapeutic effects of exogenous H2S in the experimental models of retinal photodamage in vivo and in vitro. Methods: Rats with open eyelids were pretreated with H2S (80~120 μmol/kg) for 10 days and then continuously exposed to blue light (435~445nm, 11.2W/m2) for 8 h to establish in vivo experimental model. ARPE-19 cells were pretreated with H2S and then exposed to blue light to establish in vitro experimental model. Results: In vivo experiments, H2S significantly ameliorated blue light-induced retinal oxidative stress, apoptosis and degeneration. Moreover, H2S inhibited the activation of blue light-induced endoplasmic reticulum (ER) stress CHOP apoptotic signaling. In vitro experiments, H2S improved blue light-induced oxidative stress and oxidative damage. H2S inhibited ROS-mediated activation of ER stress CHOP apoptotic signaling. H2S alleviated blue light-induced apoptosis and increases cell viability. The ER stress inhibitor 4-PBA alleviated blue light-induced apoptosis and increases cell viability. Conclusion: Taken together, these results indicate that H2S can inhibit ROS-mediated ER stress-CHOP apoptosis signal, thereby alleviating blue light-triggered retinal apoptosis and degeneration.
硫化氢通过抑制ros介导的内质网应激- chop凋亡信号保护视网膜免受蓝光诱导的光损伤和变性
背景:硫化氢(H2S)是一种小型还原性气体分子,具有抗氧化、抗凋亡、抗炎等多种生物学功能。在本研究中,我们研究了外源性H2S对视网膜光损伤实验模型的体内和体外治疗作用。方法:用H2S (80~120 μmol/kg)预处理裸眼大鼠10 d,然后连续暴露于435~445nm、11.2W/m2的蓝光下8 h,建立体内实验模型。用H2S预处理ARPE-19细胞,然后蓝光照射建立体外实验模型。结果:在体内实验中,H2S可显著改善蓝光诱导的视网膜氧化应激、细胞凋亡和变性。H2S抑制蓝光诱导内质网(ER)应激CHOP凋亡信号的激活。体外实验中,H2S可改善蓝光诱导的氧化应激和氧化损伤。H2S抑制ros介导的内质网应激CHOP凋亡信号的激活。H2S可减轻蓝光诱导的细胞凋亡,提高细胞活力。内质网应激抑制剂4-PBA可减轻蓝光诱导的细胞凋亡,提高细胞活力。结论:综上所述,H2S可抑制ros介导的ER应激- chop凋亡信号,从而减轻蓝光引发的视网膜凋亡和变性。
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来源期刊
Redox Report
Redox Report 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
28
审稿时长
>12 weeks
期刊介绍: Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
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