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活化素A对百草枯所诱导的PC12细胞损伤的保护作用
引用本文:刘楠,蒋雨平,王坚,丁正同. 活化素A对百草枯所诱导的PC12细胞损伤的保护作用[J]. 中国临床神经科学, 2006, 14(1): 25-32
作者姓名:刘楠  蒋雨平  王坚  丁正同
作者单位:1. 复旦大学神经病学研究所,200040
2. 复旦大学上海医学院神经病学系,200032
摘    要:目的:观察重组人活化素A(rhAct)对百草枯所诱导的PC12细胞损伤的保护作用。方法:将百草枯、活化素A、Ldeprenyl加入体外培养的PC12细胞中,用四甲基偶氮唑盐(MTT)法检测细胞活力的变化;免疫细胞化学法和RTPCR评价细胞的酪氨酸羟化酶和Bcl2蛋白及mRNA表达水平的变化,脱氧核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测细胞凋亡的变化,比较各组的差异。结果:预先给予活化素A和Ldeprenyl的两组细胞活力明显高于百草枯损害组,酪氨酸羟化酶和Bcl2蛋白及mRNA的表达强于损害组,同时两组的凋亡细胞明显减少,活化素A和Ldeprenyl两组间无显著差异。结论:活化素A和Ldeprenyl通过上调Bcl2的表达,抑制凋亡的发生,而对百草枯所诱导的PC12细胞损伤具有保护作用。

关 键 词:活化素A  PC12细胞  帕金森病  百草枯
文章编号:1008-0678(2006)01-0025-08
修稿时间:2004-12-27

Protective Effect of Activin A to the Injury of PC12 Cells Induced by Paraquat
LIU Nan,JIANG Yu-Ping,WANG Jian,DING Zheng-Tong. Protective Effect of Activin A to the Injury of PC12 Cells Induced by Paraquat[J]. Chinese Journal of Clinical Neurosciences, 2006, 14(1): 25-32
Authors:LIU Nan  JIANG Yu-Ping  WANG Jian  DING Zheng-Tong
Abstract:Aim:To observe the protective effect of recombinant human activin A(rhAct A)and L-deprenyl to the PC12 cells injury induced by paraquat.Methods:Paraquat,activin A or L-deprenyl was added to the culture media of PC12 cells. We assayed the cell viability with MTT method,evaluated the change of expression of protein and mRNA of tyrosine hydroxylase and Bcl-2 with immunocytochemistry and RT-PCR techniques respectively,then we investigated the number of apoptotic cells with terminal-deoxynucleotidyl transferase mediated nick end labeling(TUNEL) method. The difference between the groups was compared.Results:In the group of activin A or L-deprenyl,the cell viability was higher than that treated only with paraquat,the expression of protein and mRNA of tyrosine hydroxylase and Bcl-2 was also greater than the injuried group and the number of apoptotic cells was decreased significantly. No observable difference occurred between activin A and L-deprenyl group.Conclusion:rhAct A and L-deprenyl may have a protective effect to the injury of PC12 cells induced by paraquat via upregulating Bcl-2 expression and inhibiting apoptosis.
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