|本期目录/Table of Contents|

[1]纳 莉,徐支芳,巩慧慧,等.同型半胱氨酸致动脉粥样硬化的机制研究[J].宁夏医科大学学报,2012,(09):887-889,902.
 NA Li,XU Zhi-fang,GONG Hui-hui,et al.Induced Hyperhommocysteinemia in the Study of the Mechanisms of Otherosclerosis[J].Ningxia Medical University,2012,(09):887-889,902.
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同型半胱氨酸致动脉粥样硬化的机制研究(PDF)
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《宁夏医科大学学报》[ISSN:1005-8486/CN:64-1029/R]

卷:
期数:
2012年09期
页码:
887-889,902
栏目:
论著
出版日期:
2012-09-30

文章信息/Info

Title:
Induced Hyperhommocysteinemia in the Study of the Mechanisms of Otherosclerosis
作者:
纳 莉1 徐支芳2 巩慧慧2 孙炜炜2 梁 宇2 姜怡邓2
1.宁夏医科大学总医院外科学研究室,银川 750004; 2.宁夏医科大学,银川 750004
Author(s):
NA Li1 XU Zhi-fang2 GONG Hui-hui2 SUN Wei-wei2 LIANG Yu2 JIANG Yi-deng2
1.The Suryery Laboratory of General Hospital of Ningxia Medical University, Yinchuan 750004; 2.Ningxia Medical University,Yinchuan 750004
关键词:
同型半胱氨酸 氧化应激损伤 动脉粥样硬化
Keywords:
homocysteine oxidative stress impair atherosclerosis
分类号:
R541.4
DOI:
-
文献标志码:
A
摘要:
目的 通过观察不同浓度同型半胱氨酸(Homocysteine, Hcy)干预对人脐静脉血管内皮细胞(Human Umbilical Vein Endothelial Cells, HUVEC)和氧化应激的影响,探讨其在动脉粥样硬化(Atherosclerosis, AS)中的作用。方法 体外培养HUVEC,将其分为正常对照组(Hcy 0μmol·L-1)、Hcy干预组(浓度分别为50、100、200、500μmol·L-1)、100μM Hcy+叶酸+VitB12治疗组,每个浓度组再分为24、48、72h三个时间组。MTT法检测各组细胞增殖抑制率,测定各浓度Hcy干预HUVEC 72h的氧化应激损伤指标。结果 各浓度Hcy干预组随着Hcy浓度增高及干预时间延长HUVEC的细胞增殖抑制率增加, 500μM Hcy 72h干预组最明显(P<0.05)。HUVEC内H2O2 和MDA含量随Hcy浓度的增加而增加,Hcy100~500μM组与对照组比较差异均有统计学意义(P<0.01); Hcy100~500μM组HUVEC内SOD活性和T-AOC活性均较对照组降低(P<0.01),并且Hcy的浓度越高降低程度越明显。100μM Hcy+叶酸+VitB12治疗组与对照组比较上述各指标的差异均无统计学意义(P>0.05)。结论 Hcy抑制HUVEC增殖的作用呈剂量依赖关系,病理水平Hcy可以增强氧化应激损伤反应,而叶酸和VitB12对Hcy所致氧化应激损伤有一定的拮抗作用。
Abstract:
Objective To observe the effects of different concentrations of homocysteine(Homocysteine, Hcy)intervention on human umbilical vein endothelial cells(Human umbilical vein endothelial cells, HUVEC)and the effect of oxidative stress, and to explore its mechanisms in atherosclerosis(Atherosclerosis, AS)in rats. Methods HUVEC were cultured in vitro, which could be divided into the normal control group(Hcy 0μmol·L-1), Hcy group(concentrations were 50, 100, 200, 500 μmol·L-1), 100 μM Hcy+VitB12 of folic acid treatment group. The concentration of each group was further divided into 24h, 48h, 72h group. Cell proliferation inhibition was detected by MTT. Results HUVEC cell proliferation inhibition rate increased, 500 μM Hcy 72h group was the most(P<0.05)while the concentration of Hcy group with the Hcy concentration increased and intervention time prolonged. HUVEC H2O2 and MDA content increased as the concentration of Hcy increased(P<0.01 ); Hcy100 ~ 500μM group HUVEC SOD activity and T-AOC activity were lower than those in control group(P<0.01). 100 μM Hcy+ VitB12 of folic acid treatment group compared with the control group the differences of each index were not statistically significant(P>0.05). Conclusion The Hcy inhibit HUVEC proliferation showed a dose dependent relationship. Pathological levels of Hcy could enhance oxidative stress response to injury. Folic acid and VitB12 has certain antagonism against Hcy induced oxidative stress injury.

参考文献/References:

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备注/Memo

备注/Memo:
收稿日期:2012-01-31 作者简介:纳莉(1981- ),女,宁夏人,在读硕士研究生,主要从事心血管疾病的基础病理生理研究。 通信作者:姜怡邓(1974-),男,湖南人,副教授,硕士研究生导师,博士,从事动脉粥样硬化分子机制的研究。E-mail: jwcjyd@163. com
更新日期/Last Update: 2012-09-20