【打印本页】 【下载PDF全文】 【HTML】 查看/发表评论下载PDF阅读器关闭

←前一篇|后一篇→

过刊浏览    高级检索

本文已被:浏览 2386次   下载 2610 本文二维码信息
码上扫一扫!
甘氨酸对氧糖剥夺诱导大鼠神经元损伤的抗凋亡作用
林莉莉1,赵蕾2*,姚雯1,邹浩军1
0
(1.无锡卫生高等职业技术学校药理学教研室,无锡 214028
2.第二军医大学研究生院,上海 200433
*通信作者)
摘要:
目的 探讨甘氨酸对氧糖剥夺诱导神经元损伤的作用及机制。方法 采用体外培养的大鼠原代神经元建立氧糖剥夺模型,随机分为正常对照组、氧糖剥夺组和甘氨酸处理组,应用MTT、流式细胞术等方法检测甘氨酸对神经元活性、生存率、细胞凋亡的影响; 应用蛋白质印迹测定甘氨酸对凋亡蛋白Bcl-2、Bcl-xL、Bad、Bax的影响。结果 甘氨酸能够提高大鼠原代神经元活力和存活率,减少细胞凋亡,并且能够增加抗凋亡因子Bcl-2,降低促凋亡因子Bax的表达(P<0.05或P<0.01)。结论 甘氨酸对氧糖剥夺神经元有明显的保护作用,该作用可能与促进抗凋亡因子、抑制促凋亡因子释放有关。
关键词:  甘氨酸  神经元  氧糖剥夺  细胞凋亡
DOI:
投稿时间:2013-04-08修订日期:2013-08-20
基金项目:江苏省教育厅高校“青蓝工程”优秀青年骨干教师基金, 无锡市医院管理中心医学重点人才“导师制”基金.
Anti-apoptotic effects of glycine against neuron injury induced by oxygen glucose deprivation
LIN Li-li1,ZHAO Lei2*,YAO Wen1,ZOU Hao-jun1
(1. Department of Pharmacology, Wuxi Higher Health Vocational Technology School, Wuxi 214028, Jiangsu, China
2. Postgraduate College, Second Military Medical University, Shanghai 200433, China
*Corresponding author.)
Abstract:
Objective To investigate the effects of glycine on neuron injury induced by oxygen glucose deprivation (OGD) and the underlying mechanisms. Methods In vitro OGD model was established with cultured rat primary neurons. The study was randomly divided into normal control group, OGD group and glycine treatment group. The influences of glycine on cell activity and survival rate were detected by MTT, and cell apoptosis was detected by flow cytometry. Western blotting analysis was used to examine the effect of glycine on expression of apoptotic proteins Bcl-2, Bcl-xL, Bad, and Bax. Results Glycine could improve the activity and survival of primary neurons of rats and decrease neuron apoptosis. Glycine also significantly increased anti-apoptotic proteins Bcl-2 expression and significantly decreased pro-apoptotic proteins Bax expression (P<0.05 or P<0.01). Conclusion Glycine can notably alleviate neuron injury induced by OGD, which is probably through up-regulation of anti-apoptotic factors and down-regulation of pro-apoptotic factors.
Key words:  glycine  neurons  oxygen glucose deprivation  apoptosis