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目的 观察抗微管药物紫杉醇对T细胞淋巴瘤细胞株Jurkat是否具有凋亡诱导作用 ,并进一步研究bcl 2基因家族在此过程中的作用。方法 将不同浓度的紫杉醇作用于Jurkat细胞 ,观察其作用的时间效应及剂量效应 ;在光镜和电镜下观察其形态变化 ;用流式细胞术分析细胞DNA含量的改变并作DNA片段分析 ;用免疫组织化学及半定量逆转录 聚合酶链反应 (RT PCR)法观察在紫杉醇作用过程中凋亡调节基因bcl 2家族的mRNA和蛋白表达的变化。结果 紫杉醇能抑制Jurkat细胞生长 ,在一定剂量和时间范围内 ,主要引起细胞凋亡 ,并显示剂量和时间效应 ,在这个过程中bax转录及蛋白表达增加 ,并出现bcl xs的转录。结论 紫杉醇能特异地诱导Jurkat细胞凋亡 ,这为紫杉醇应用于T细胞淋巴瘤的治疗提供了依据 ,并为研究淋巴瘤细胞凋亡的基因调控提供了极好的模型 ,bax和bcl xs参与了紫杉醇诱导Jurkat细胞凋亡的基因调控。
Objective To investigate whether anti-microtubule paclitaxel induces apoptosis in T lymphocyte cell line Jurkat and to further investigate the role of bcl 2 gene family in this process. Methods Different concentrations of paclitaxel were applied to Jurkat cells to observe their time effect and dose effect. Morphological changes were observed under light microscope and electron microscope. The changes of DNA content were analyzed by flow cytometry and DNA fragments were analyzed. Immunohistochemistry and semiquantitative reverse transcription polymerase chain reaction (RT PCR) method were used to observe the changes of mRNA and protein expression of apoptosis-regulating gene bcl 2 family during paclitaxel treatment. Results Paclitaxel could inhibit the growth of Jurkat cells. Under certain dose and time range, paclitaxel mainly induced apoptosis and showed dose and time effects. During this process, bax transcription and protein expression increased, and the transcription of bcl xs appeared. Conclusion Paclitaxel can specifically induce apoptosis of Jurkat cells, which provides a basis for the application of paclitaxel in the treatment of T-cell lymphoma and provides an excellent model for studying the gene regulation of apoptosis of lymphoma cells. Bax and bcl xs are involved Gene regulation of paclitaxel - induced Jurkat cell.