[1]杨丽娟,邬力祥,李伟,等.17β-雌二醇对氧糖剥夺神经元的保护作用[J].第三军医大学学报,2009,31(07):585-588.
 YANG Li-juan,WU Li-xiang,LI Wei,et al.17β-estradiol pretreatment protects rat cortical neurons injured by oxygen-glucose deprivation in vitro[J].J Third Mil Med Univ,2009,31(07):585-588.
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17β-雌二醇对氧糖剥夺神经元的保护作用(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
31卷
期数:
2009年第07期
页码:
585-588
栏目:
论著
出版日期:
2009-04-15

文章信息/Info

Title:
17β-estradiol pretreatment protects rat cortical neurons injured by oxygen-glucose deprivation in vitro
作者:
杨丽娟邬力祥李伟贺芳张琰黄柏胜
中南大学湘雅医学院生理学系;滨州医学院:生理教研室,附属医院胸心外科
Author(s):
YANG Li-juan WU Li-xiang LI Wei HE Fang ZHANG Yan HUANG Bo-sheng
Department of Physiology, Xiangya School of Medicine, Central South University, Changsha 410078; Department of Physiology, Affiliated Hospital,  Department of Cardiotharasis Surgery, Binzhou Medical College, Binzhou 256603, Shandong Province, China
关键词:
17β-雌二醇神经元葡萄糖自由基
Keywords:
17β-estradiol neurons oxygen glucose free radicals
分类号:
R322.81;R329.28;R977.1
文献标志码:
A
摘要:
目的    研究17β-雌二醇(17β-estradiol,E2)对氧糖剥夺大鼠皮层神经元的保护作用。    方法    体外培养鼠脑皮层神经元,建立缺血缺氧模型。利用MTT代谢法、流式细胞术和Hoechst 33342荧光染色观察E2(10-8mol/L)对缺氧损伤皮层神经元细胞活力和凋亡的影响;硫代巴比妥酸法测定丙二醛(MDA)含量,黄嘌呤氧化酶法测超氧化物歧化酶(SOD)活力变化。    结果    氧糖剥夺后神经元细胞活力显著降低,凋亡率升高,MDA生成增多,SOD的活力下降,与空白对照组相比有统计学差异(P<0.05);E2预处理后细胞活力升高、凋亡率下降、MDA生成减少、SOD的活性升高,与氧糖剥夺组相比有统计学差异(P<0.01)。    结论    E2对氧糖剥夺神经元具有保护作用,其作用可能与SOD活性提高拮抗氧自由基对细胞的损伤有关。
Abstract:
Objective    To explore the effect of 17β-estradiol on rat cortical neurons injured by oxygenglucose deprivation (OGD).     Methods    Primary cortical neurons were isolated from neonatal rats and identified with NSE staining, then cultured for 10 d under normal condition. To establish OGD injury, the culture medium was replaced by glucose-free medium, and cells were transferred to a humidified incubation chamber flushed by a gas mixture of 95% N2 and 5% CO2 at 37 ℃ for 2 h. To explore the influence of 17β-estradiol on neurons under OGD for 2 h condition, the cells were pretreated with 10-8 mol/L 17β-estradiol 24 h prior to OGD. The cell viability were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the percentage of apoptotic cells was tested by flow cytometry and Hoechst 33342 staining. The contents of MDA and the activities of SOD were evaluated by biochemical methods.     Results    The results showed that OGD injury significantly decreased the cell viability and the activities of SOD, increased the percentage of apoptotic cells and the content of MDA (P<0.05). Pretreament of 10-8mol/L 17β-estradiol increased the cell viability and the activities of SOD, decreased the contents of MDA and the percentage of apoptotic cells in cortical neurons exposure to OGD (P<0.01).     Conclusion    17β-estradiol has the neuroprotective effect on cortical neurons after OGD injury. This effect of 17β-estradiol may be mediated by eliminating the free radicals by increasing the activities of antioxidative enzymes and thus inhibit the oxidative damages caused by OGD.

参考文献/References:

杨丽娟,邬力祥,李伟,等. 17β-雌二醇对氧糖剥夺神经元的保护作用[J]. 第三军医大学学报,2009,31(7):585-588.

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更新日期/Last Update: 2009-04-15