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-.

• 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
  • 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
  • 作者简介:刘乃榕（1990-），女，医学硕士，助教。研究方向：营养与慢性病防治
  • 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
  • Published:2021-04-25 Online:2021-05-18

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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