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首页> 外文期刊>Current Eye Research >Protective Effects of Trimetazidine in Retarding Selenite-Induced Lens Opacification
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Protective Effects of Trimetazidine in Retarding Selenite-Induced Lens Opacification

机译：三种嗪对旋转硒诱导透镜透明化透镜透明化的保护作用

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摘要

Purpose: Cataracts are the leading cause of vision loss worldwide, and the over-production of reactive oxygen species (ROS) is the foremost underlying cause of cataracts. Reducing ROS levels can efficiently prevent lens opacification, as evidenced by many studies. Here, we inhibited ROS overproduction with trimetazidine (TMZ), which is an antioxidant, to explore the therapeutic effects of TMZ and the mechanism of lens opacification. Materials and methods: Sodium selenite-induced cataract formation resulted in a significant loss of lens transparency. This effect could be efficiently rescued by TMZ, which was further found to be an inhibitor of ROS production, as determined by assaying oxidative stress-related parameters (SOD activity, MDA, center dot OH and H2O2 levels) during cataract formation. The experimental protocols involving animal research were approved by the Animal Care and Ethics Committee of Wenzhou Medical University and conducted according to the Association for Research in Vision and Ophthalmology under the guidelines of the Animal Welfare Act (SYXK 2015-0009). Results: Our study found that TMZ can retard the onset and progression of lens opacification in vivo in experiments using Sprague-Dawley (SD) suckling rats and can rescue the morphology of HLEB3 cells in vitro. The flow cytometry and DNA fragmentation assays showed that TMZ could prevent sodium selenite-induced apoptosis. The western blot analysing showed that the levels of apoptosis-associated Bcl-2 and Nrf2 were dramatically decreased following the sodium selenite treatment. In addition, the bisulfate DNA sequencing revealed that the demethylation of CpGs in the promoter region of Keap1 was stimulated, and that this demethylation could be inhibited by TMZ by rescuing the Nrf2 expression level. Conclusions: Our findings indicate that the antioxidant TMZ strongly reduces ROS production, which ultimately delays the progression of cataract formation, suggesting that treatment with TMZ represents a novel, promising antioxidant protection to retard cataract formation.
机译：目的：白内障是全球视力丧失的主要原因，反应性氧物种（ROS）的过度生产是白内障的最重要原因。减少ROS水平可以有效地防止透镜透明化，如许多研究所证明。在此，我们抑制了甲嗪（TMZ）的ROS生产，即抗氧化剂，以探讨TMZ的治疗效果和透镜透明度的机制。材料和方法：硒沸石诱导的白内障地层导致透镜透明度的显着损失。通过TMZ可以有效地拯救该效果，该效果进一步发现是ROS产生的抑制剂，如通过在白内障地层期间测定氧化应激相关参数（SOD活性，MDA，中心点OH和H2O2水平）来确定。涉及动物研究的实验方案由温州医科大学的动物护理和伦理委员会批准，并根据“动物福利法”指导方针（SYXK 2015-0009）的视力和眼科研究协会进行。结果：我们的研究发现，TMZ可以在使用Sprague-Dawley（SD）哺乳大鼠的实验中延缓体内晶状体透镜的发作和进展，并且可以在体外拯救HELB3细胞的形态。流式细胞术和DNA碎片测定显示TMZ可以预防硒沸石诱导的细胞凋亡。 Western Blot分析表明，在硒沸石治疗钠的情况下，凋亡相关的Bcl-2和NRF2的水平显着降低。此外，苯磺酸盐DNA测序显示刺激Keap1的启动子区中CpG的去甲基化，并且通过借鉴NRF2表达水平，可以通过TMZ抑制该去甲基化。结论：我们的研究结果表明，抗氧化剂TMZ强烈降低了ROS生产，最终延迟了白内障地层的进展，表明用TMZ治疗代表了一种新颖，有前途的抗氧化保护，以延迟白内障形成。

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  • 来源
    《Current Eye Research》 |2019年第12期|共12页
  • 作者

    Fang Weifang; Ye Qin; Yao Yihua; Xiu Yanghui; Gu Feng; Zhu Yihua;

  • 作者单位

    Fujian Med Univ Affiliated Hosp 1 Dept Ophthalmol Fuzhou 350005 Fujian Peoples R China;

    Fujian Med Univ Affiliated Hosp 1 Dept Ophthalmol Fuzhou 350005 Fujian Peoples R China;

    Fujian Med Univ Affiliated Hosp 1 Dept Ophthalmol Fuzhou 350005 Fujian Peoples R China;

    Affiliated Xiamen Univ Eye Inst Xiamen Fujian Peoples R China;

    Wenzhou Med Univ Eye Hosp Sch Ophthalmol &

    Optometry State Key Lab Cultivat Base Wenzhou;

    Fujian Med Univ Affiliated Hosp 1 Dept Ophthalmol Fuzhou 350005 Fujian Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 眼科学;
  • 关键词

    Cataract; Trimetazidine (TMZ); reactive oxygen species; Keap1; Nrf2 pathway;

    机译：白内障;三嗪（TMZ）;活性氧物种;Keap1;NRF2途径;

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