子查询返回的值不止一个。当子查询跟随在 =、!=、<、<=、>、>= 之后，或子查询用作表达式时，这种情况是不允许的。 同型半胱氨酸对小鼠成神经瘤细胞毒性作用研究-《天津医科大学学报》
|本期目录/Table of Contents|

[1]苟 芸,黄国伟,陈 爽,等.同型半胱氨酸对小鼠成神经瘤细胞毒性作用研究[J].天津医科大学学报,2015,21(03):6-8.
　GOU Yun,HUANG Guo-wei,CHEN Shuang,et al.Neurotoxicity of homocysteine on mouse N2a neuroblastoma cells[J].Journal of Tianjin Medical University,2015,21(03):6-8.
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同型半胱氨酸对小鼠成神经瘤细胞毒性作用研究(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
21卷
期数:
2015年03期
页码:
6-8
栏目:
基础医学
出版日期:
2015-05-20

文章信息/Info

Title:
Neurotoxicity of homocysteine on mouse N2a neuroblastoma cells
文章编号:
1006-8147（2015）0-0006-03
作者:

苟 芸;  黄国伟;  陈 爽;  张绪梅

（天津医科大学公共卫生学院营养与食品卫生学系，天津 300070）

Author(s):
GOU Yun;  HUANG Guo-wei;  CHEN Shuang;  ZHANG Xu-mei
(Department of Nutrition and Food Hygiene, School of Public Health, Tianjin Medical University, Tianjin 300070, China)
关键词:
同型半胱氨酸; 小鼠; 成神经瘤细胞N2a; 细胞凋亡; pERK1/2
Keywords:
homocysteine;  mouse;  N2a;  cell apoptosis;  pERK1/2
分类号:
R15
DOI:
-
文献标志码:
A
摘要:
 目的：研究同型半胱氨酸（Hcy）对小鼠成神经瘤细胞（N2a）毒性作用并探讨其对pERK1/2蛋白表达的影响。 方法： 培养的N2a细胞加入不同浓度Hcy，随机分为4组：分别为正常对照组及Hcy低、Hcy中、Hcy高浓度组，根据预实验结果确定以上4组Hcy干预浓度分别为 0、 30、300和 1 000 μmol/L。作用72 h后，用酶标仪测定细胞培养液中乳酸脱氢酶（LDH）活性，MTT法检测细胞增殖情况，蛋白质免疫印迹法检测N2a细胞pERK1/2蛋白表达水平。 结果： 与正常对照组相比，Hcy低、中、高浓度组细胞培养液中LDH活性均显著升高，差异具有统计学意义（P值分别为0.013、0.008和0.011， P<0.05）。低、中、高浓度Hcy作用后，MTT检测细胞增殖活力下降，OD值降低，与对照组比较，差异具有统计学意义（P值分别为0.01、0.006和0.009， P<0.05）。各Hcy干预组pERK1/2蛋白表达量降低，且中、高浓度Hcy组pERK1/2蛋白表达量与对照组相比差异具有统计学意义（P值分别为0.038、0.007， P<0.05）。 结论： Hcy能抑制磷酸化的ERK1/2蛋白表达，从而对N2a产生毒性作用，进而抑制N2a增殖，提示降低血清中Hcy水平可以对神经细胞产生保护作用。
Abstract:
Objective: To explore the neurotoxicity of homocysteine on mouse neuroblastoma cells (N2a) and its effect on pERK1/2 protein level. Methods: Cultured N2a cells were divided into four groups according to the concentrations of homocysteine: control group (0 μmol/L), low-Hcy (30 μmol/L), moderate-Hcy (300 μmol/L), high-Hcy (1 000 μmol/L) groups. After 72 h Hcy treatment, the toxicity of N2a cells was detected by LDH (lacate dehydrogenase) assay kit, cell proliferation ability was detected by MTT methods, and the protein expression of pERK1/2 was detected by western blot. Results: The LDH activity in Hcy-treated groups was increased compared with control group (P<0.05). The cells proliferation ability was decreased after Hcy treatment, and OD values were reduced compared with control group (P<0.05). The protein expression of pERK1/2 decreased after Hcy treatment, and significant differences among the moderate, high Hcy dose groups and control group were found (P<0.05). Conclusion: The toxic effect of Hcy on N2a cells may be caused by reduced ERK1/2 protein phosphorylation expression. It suggests that a low serum Hcy level may have a protective effect on neural cells.

参考文献/References:

[1]Herrmann W, Obeid R. Homocysteine: a biomarker in neurodegenerative diseases[J]. Clin Chem Lab Med, 2011, 49(3): 435

[2]Schalinske K L, Smazal A L. Homocysteine imbalance: a pathological metabolic marker[J]. Adv Nutr, 2012, 3(6): 755

[3]Wang Fang, Wang Jianhua, Guo Jin, et al. PCMT1 gene polymorphisms, maternal folate metabolism, and neural tube defects: a case-control study in a population with relatively low folate intake[J]. Genes Nutr, 2013, 8(6): 581

[4]Lominadze D, Tyagi N, Sen U, et al. Homocysteine alters cerebral microvascular integrity and causes remodeling by antagonizing GABA-A receptor[J]. Mol Cell Biochem, 2012, 371(1/2): 89.

[5]Ataie Amin, Ataee Ramin, Shadifar M, et al. Interaction of memantine with homocysteine on the apoptosis in the rat hippocampus cells[J]. Int J Mol Cell Med, 2012, 1(3): 145

[6]Lee S J, Kang M H, Min H. Folic acid supplementation reduces oxidative stress and hepatic toxicity in rats treated chronically with ethanol[J]. Nutr Res Pract, 2011, 5(6): 520

[7]Fiorito G, Guarrera S, Valle C, et al. B-vitamins intake, DNA-methylation of One Carbon Metabolism and homocysteine pathway genes and myocardial infarction risk: the EPICOR study[J]. Nutr Metab Cardiovasc Dis, 2014, 24(5): 483

[8]Guo Hang YUAN, Xu Fu KANG, Lv Hai TAO, et al. Hyperhomocysteinemia independently causes and promotes atherosclerosis in LDL receptor-deficient mice[J]. J Geriatr Cardiol, 2014, 11(1): 74

[9]程丝，冯娟，王宪．高同型半胱氨酸血症治疗研究进展[J]．生理科学进展，2011，42（5）：329

[10]Parmar M S, Jaumotte J D, Wyrostek S L, et al. Role of ERK1, 2, and 5 in dopamine neuron survival during aging[J]. Neurobiol Aging, 2014, 35(3): 669

[11]Matteucci A, Gaddini L, Villa M, et al. Neuroprotection by rat Müller glia against high glucose-induced neurodegeneration through a mechanism involving ERK1/2 activation[J]. Exp Eye Res, 2014, 125 : 20

[12]Yang Kun, Cao Fujiang, Sheikh A M, et al. Up-regulation of Ras/Raf/ERK1/2 signaling impairs cultured neuronal cell migration, neurogenesis, synapse formation, and dendritic spine development[J]. Brain Struct Funct, 2013, 218(3): 669

[13]Ortuño-Sahagún D, González R M, Verdaguer E, et al. Glutamate excitotoxicity activates the MAPK/ERK signaling pathway and induces the survival of rat hippocampal neurons in vivo[J]. J Mol Neurosci, 2014, 52(3): 366

[14]Türkcü F M, Köz O G, Yarangümeli A, et al. Plasma homocysteine, folic acid, and vitamin B?? levels in patients with pseudoexfoliation syndrome, pseudoexfoliation glaucoma, and normotensive glaucoma[J]. Medicina (Kaunas), 2013, 49(5): 214

[15]Zhang Xu MEI, Huang Guo WEI, Tian Zhi HONG, et al. Folate stimulates ERK1/2 phosphorylation and cell proliferation in fetal neural stem cells[J]. Nutr Neurosci, 2009, 12(5): 226

[16]Zhang Xu MEI, Huang Guo WEI, Tian Zhi HONG, et al. Folate deficiency induces neural stem cell apoptosis by increasing homocysteine in vitro[J]. J Clin Biochem Nutr, 2009, 45(1): 14

[17]Cao Hui, Hu Xinhua, Zhang Qiang, et al. Hyperhomocysteinaemia, low folate concentrations and MTHFR C677T mutation in abdominal aortic aneurysm[J]. Vasa, 2014, 43(3): 181

[18]周小红，刘向一．脑梗赛患者血清叶酸浓度的改变[J]．中华临床医学杂志，2006，7（8）：49

 

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备注/Memo

备注/Memo:

基金项目 国家自然科学基金资助项目（81373003）； 中国博士后科学基金（2014M550148 )

作者简介 苟芸（1990-），女， 硕士在读，研究方向：营养与神经退行性疾病；通信作者：张绪梅，E-mail: zhangxumei@tijmu.edu.cn 。

更新日期/Last Update: 2015-01-22