ISSN 1674-3865  CN 21-1569/R
主管：国家卫生健康委员会
主办：中国医师协会
　　　辽宁省基础医学研究所
　　　辽宁中医药大学附属医院
中国中西医结合儿科学

中国中西医结合儿科学 ›› 2021, Vol. 13 ›› Issue (2): 99-.doi: 10.3969/j.issn.1674-3865.2021.02.003

• 实验论著 • 上一篇    下一篇

维生素B12早期干预影响海马神经元DNA甲基化和抗β淀粉样蛋白神经毒性作用

刘乃榕，李景辉，任刚，李晶，詹杰   

  1. 110000 沈阳，辽宁医药职业学院医学营养教研室
  • 收稿日期:2020-11-05 出版日期:2021-04-25 上线日期:2021-05-18
  • 通讯作者: 詹杰，E-mail：2424485544@qq.com
  • 基金资助:
    辽宁省科学事业公益研究基金计划项目（20170032）

Effect of vitamin  B12 early intervention on DNA methylation and Aβ neurotoxicity of hippocampal neuron cells

LIU Nairong，LI Jinghui，REN Gang，LI Jing，ZHAN Jie   

  1.  Liaoning Vocational College of Medicine，Shenyang 110000，China
  • Received:2020-11-05 Published:2021-04-25 Online:2021-05-18
  • Contact: ZHAN Jie，E-mail：2424485544@qq.com

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摘要： 目的：探索生命早期补充维生素B12对海马神经元细胞（HNCs）DNA甲基化水平及抗β淀粉样蛋白（Aβ）毒性的作用及机制。方法：新生大鼠出生12 h内取HNCs体外培养，随机分为空白组、模型组及维生素B12低、中、高剂量组，进行不同剂量维生素B12干预，HPLC法测定DNA甲基化水平，同时观察生命早期维生素B12干预对成熟期HNCs细胞Aβ1-42染毒后细胞增殖率、细胞凋亡率、丙二醛含量、超氧化物歧化酶（SOD）活力和谷胱甘肽过氧化物酶（GSH-PX）活力的影响。结果：维生素B12早期干预HNCs细胞DNA甲基化水平较空白组明显降低，差异有统计学意义（P<0.05）；Aβ染毒可造成HNCs细胞增殖率显著下降、细胞凋亡率明显升高、丙二醛含量增高、SOD活力和GSH-PX活力降低，差异有统计学意义（P<0.05）。与模型组比较，生命早期补充维生素B12可提高成熟期HNCs细胞Aβ染毒后的细胞增殖率，降低细胞凋亡率，减少丙二醛含量，增加SOD和GSH-PX活力，差异有统计学意义（P<0.05）。结论：维生素B12生命早期干预，有助于降低神经元细胞的甲基化水平，并在成熟期神经元细胞发挥对抗Aβ神经毒性作用，参与神经元细胞氧化应激，促进细胞增殖，减缓神经细胞凋亡

关键词: 阿尔茨海默病, 维生素B12, DNA甲基化, 预防

Abstract: Objective：To explore the effect of vitamin  B12 supplementation in early life on DNA methylation level and Aβ toxicity in hippocampal neuron cells(HNCs) and its mechanism.Methods：HNCs in 12 h of birth of the newborn rats were taken for culture in vitro, which were randomly divided into 5 groups: blank group, model group, low dosage vitamin  B12 group, medium-dosage group and high-dosage group. Different dosages of vitamin  B12 were given for intervention. HPLC method was used to determine the level of DNA methylation; meanwhile, observe the effect of early intervention by vitamin  B12 on proliferation rate(PR) and apoptosis rate(AR) of mature HNCs after Aβ1-42  toxification, MDA content, SOD activity and GSH-PX activity.Results：The DNA methylation level of HNCs intervened by vitamin  B12 at early stage was significantly lower than the control group(P<0.05);Aβ toxification could significantly decrease the PR and increase the AR of HNCs, and increase MDA content and reduce the activity of SOD and GSH-PX(P<0.05). Compared with model group, vitamin  B12 supplementation in early life could increase PR of mature HNCs after Aβ toxification, decrease the AR, reduce MDA content, and increase the activity of SOD and GSH-PX, the difference being statistical((P<0.05).Conclusion:Supplementation of vitamin  B12  in early life is helpful to decrease the methylation level of neuron cells, which plays an anti-Aβ neurotoxicity role in mature neuron cells, participates in oxidative stress of neuron cells, promotes cell proliferation and slows down apoptosis of neuron cells.

Key words: Alzheimer disease;Vitamin , B12;DNA methylation;Prevention