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地塞米松干预大鼠星形胶质细胞周期素的表达及细胞周期进程
引用本文:欧阳铭,刘晓柳,张少春. 地塞米松干预大鼠星形胶质细胞周期素的表达及细胞周期进程[J]. 中国临床康复, 2012, 0(2): 291-294
作者姓名:欧阳铭  刘晓柳  张少春
作者单位:武汉科技大学医学院,湖北省武汉市430065
摘    要:背景:有研究表明地塞米松可引起星形胶质细胞凋亡,但其机制不清,有关地塞米松干扰星形胶质细胞的周期素表达的作用未见报道。目的:观察地塞米松引起大鼠星形胶质细胞凋亡与周期素表达的关系。方法:将不同浓度的地塞米松(0,10-5,10-4,10-3mol/L)与纯化培养的大鼠大脑皮质星形胶质细胞共同孵育24h后,经流式细胞仪检测细胞周期,并用免疫细胞化学方法检测周期素A和E在星形胶质细胞内的表达。结果与结论:地塞米松10-5,10-4mol/L浓度组G1期细胞指数较对照组增加(P〈0.05,P〈0.01),10-3mol/L组的S期细胞指数较对照组明显升高(P〈0.01);周期素A的表达随着地塞米松浓度的升高而减弱(P〈0.05)。周期素E的表达在地塞米松0,10-5,10-4mol/L组随着地塞米松浓度的升高而减弱(P〈0.05),但在10-3mol/L浓度组反而表达增强(P〈0.01)。说明地塞米松10-5,10-4mol/L干预的星形胶质细胞周期进程受阻于G1期且与周期素A和E表达降低有关,地塞米松10-3mol/L干预的星形胶质细胞周期进程受阻于S期主要与周期素A表达降低有关。

关 键 词:地塞米松  星形胶质细胞  细胞周期  周期素  组织工程

Effect of dexamethasone on the cell cycle progression and cyclin expression of astrocytes in rats
Ouyang Ming,Liu Xiao-liu,Zhang Shao-chun. Effect of dexamethasone on the cell cycle progression and cyclin expression of astrocytes in rats[J]. Chinese Journal of Clinical Rehabilitation, 2012, 0(2): 291-294
Authors:Ouyang Ming  Liu Xiao-liu  Zhang Shao-chun
Affiliation:Medical College of Wuhan University of Science and Technology, Wuhan 430065, Hubei Province, China
Abstract:BACKGROUND: Studies show that the dexamethasone (DEX) can induce the apoptosis of astrocytes. However, the mechanism is not clear. There are no reports related to the interference of DEX on cyclin expression of astrocytes. OBJECTIVE: To study the relationship between apoptosis and the expression of cyclin in astrocytes of rats induced by DEX. METHODS: Pure cultured astrocytes from rat cerebral cortex were incubated with different concentrations (0, 10-5, 10-4, 10-3 mol/L) of DEX for 24 hours. The cell cycle of the astrocytes was examined by the flow cytomete. Then the expressions of cyclin A and cyclin E in astrocytes were measured by immunocytochemistry. RESULTS AND CONCLUSION: The cell index of G1 phase was obviously increased in the 10-5 and 10-4 mol/L groups (P 0.05, P 0.01), and the cell index of S phase was obviously increased in 10-3 mol/L group compared with the control group (P 0.01). The expression of cyclin A was decreased with the increasing of DEX concentration. The expression of cyclin E was decreased with the increasing of DEX concentration in the 10-5 and 10-4 mol/L groups (P 0.05), and increased in the 10-3 mol/L group (P 0.01). The attenuated expression of cyclin A and cyclin E may contribute to the cell cycle arrest at G1 phase in the 10-5 and 10-4 mol/L groups, while the cell cycle arrest at S phase in 10-3 mol/L group may mainly attribute to the attenuated expression of cyclin A.
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