伊马替尼诱导原代T细胞凋亡作用机制研究 |
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引用本文: | 陈小华 邱华云 施珊珊 吴 莎 林 晨 李扬秋. 伊马替尼诱导原代T细胞凋亡作用机制研究[J]. 中国免疫学杂志, 2016, 32(9): 1268 |
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作者姓名: | 陈小华 邱华云 施珊珊 吴 莎 林 晨 李扬秋 |
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摘 要: | 目的:研究伊马替尼(IM)诱导正常人原代CD3+ T细胞凋亡的分子机制。 方法: 0~100 nmol/L的IM作用原代T细胞24 h后,应用流式细胞术检测细胞凋亡情况;应用实时荧光定量PCR技术检测Caspase-3、Caspase-8、A20和NF-κB基因表达变化;应用Western blot技术检测A20和NF-κB蛋白表达变化。结果:IM具有明显促T细胞凋亡能力,其凋亡分子Caspase-3 和A20基因表达水平均上调,而NF-κB的基因和蛋白水平均下调。结论:IM通过上调A20的表达诱导了T细胞的凋亡。
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关 键 词: | 伊马替尼;原代CD3+ T细胞;TNF-&alpha 诱导蛋白3 核转录因子 |
Mechanisms of imatinib mesylate induced apoptosis of primary T cells |
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Abstract: | Objective:To investigate mechanism of imatinib mesylate induced apoptosis of primary CD3+T cells.Methods: The CD3+T cells were stimulated by 0-100 nmol/L imatinib for 24 h,cell apoptosis was detected by flow cytometry;Caspase-3,Caspase-8,A20 and NF-κB expression levels were detected by Real-time quantitative PCR and Western blot.Results: IM significantly increased apoptosis of T cell;Caspase-3 and A20 gene expression levels were upregulated and NF-κB expression level was downregulated both in gene and protein levels.Conclusion: IM increased apoptosis of T cell by upregulating A20 expression. |
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