生物学杂志

生物学杂志 ›› 2021, Vol. 38 ›› Issue (5): 23-.doi: 10.3969/j.issn. 2095-1736.2021.05.023

• 研究报告 • 上一篇    下一篇

敲除SOCS1a基因对斑马鱼肝脏氧化应激的影响

  

  1. 1. 广西北部湾海洋生物多样性养护重点实验室，钦州 535011；
    2. 广西大学 轻工与食品工程学院，南宁 530004；
    3.中国科学院大学 水生生物研究所 水生生物多样性与保护重点实验室， 武汉 430072；
    4.华东师范大学 生命科学学院 水生动物营养与环境健康实验室， 上海 200241
  • 出版日期:2021-10-18 发布日期:2021-10-20
  • 作者简介:戴梓茹，博士，副教授，研究方向为海洋食品资源开发与利用，E-mail：zirudai@163.com
  • 基金资助:
    广西自然科学基金青年基金项目（2016GXNSFBA380110）；广西北部湾海洋生物多样性养护重点实验室自主项目（2019ZB06）

Depletion of SOCS1a causes hepatic oxidative stress in zebrafish

  1. 1. Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, Qinzhou 535011, China;
    2. College of Light Industry and Food Engineering, Guangxi University, Nanning 530004, China;
    3. Key Laboratory of Aquatic Biodiversity and Conservation of the Chinese Academy of Sciences,
    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China;
    4. Laboratory of Aquaculture Nutrition and Environmental Health (LANEH), School of Life Sciences,
    East China Normal University, Shanghai 200241, China
  • Online:2021-10-18 Published:2021-10-20

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摘要： 为探讨SOCS1a基因敲除对斑马鱼肝脏氧化应激的影响，以SOCS1a敲除系为试验组，同胞野生型为对照组，分别采用高脂和普通饲料喂养成年斑马鱼6周后，对试验组和对照组斑马鱼的肝脏组织进行透射电镜（TEM）分析，肝脏中抗氧化酶活力测定及转录组分析。TEM结果显示：SOCS1a基因敲除的斑马鱼肝组织线粒体出现异常膨胀现象，线粒体脊密度明显减少，肝细胞中有明显的脂滴积累；抗氧化酶检测结果显示，在普通饲料饲养条件下，SOCS1a敲除组肝脏中超氧化物歧化酶（SOD）和谷胱甘肽还原酶（GR）活力分别低于野生型组27.813和3.879 U/mg(prot)。在高脂条件下，SOCS1a敲除组肝脏中SOD和GR活力分别低于野生型组14.015和3.865 U/mg(prot)；转录组数据分析显示，敲除SOCS1a基因后，导致斑马鱼肝脏氧化应激相关信号通路显著上调。敲除斑马鱼SOCS1a基因对机体造成了一定的氧化损伤，发生氧化应激反应，而在高脂诱导下，氧化应激反应更为激烈。

关键词: SOCS1a基因敲除, 斑马鱼, 高脂, 肝脏, 转录组, 氧化应激

Abstract: To investigate the effect of SOCS1a on liver oxidative stress in zebrafish, the liver tissues of zebrafish were analyzed by transmission electron microscopy (TEM), the activity of antioxidant enzymes and transcriptome between the SOCS1a-deficient adult zebrafish and their control siblings after feeding with high fat food and normal food for 6 weeks was assayed. Abnormal expansion, decreased ridge density of mitochondria and lipid droplet accumulation were observed in the liver of SOCS1a-deficient zebrafish. Under normal feed feeding conditions, the activities of superoxide dismutase (SOD) and glutathione reductase (GR) were lower in the liver of SOCS1a mutant compared with their control siblings by 27.813 and 3.879U/mg(prot), respectively. Under high-fat conditions, the SOD and GR activities were lower in the liver of SOCS1a mutant compared with their control siblings by 14.015 and 3.865 U/mg(prot), respectively. Transcriptome analysis showed the oxidative stress-related signaling pathway was significantly upregulated in the SOCS1a-deficient zebrafish. Overall, the SOCS1a knockout in zebrafish caused oxidative damage and oxidative stress, and the oxidative stress was more intense under the induction of high fat food.

Key words: SOCS1a knockout, zebrafish, hyperlipidemia, liver, transcriptome, oxidative stress

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