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首页|神经激肽受体2的拮抗剂SR48968对三种白血病细胞的作用及其作用机制的初步探讨

神经激肽受体2的拮抗剂SR48968对三种白血病细胞的作用及其作用机制的初步探讨

he effects and mechanisms of SR48968, an antagonist of neurokinin receptor 2, on three types of leukaemia cells

中文摘要英文摘要

目前研究发现在一些肿瘤细胞或肿瘤组织中神经激肽受体的表达水平会发生明显变化。SR48968是神经激肽受体2的第三代有机小分子拮抗剂。白血病是一类严重危害人类健康的疾病,本文选用人慢性粒性白血病细胞K562,人急性粒性白血病细胞HL-60和小鼠红白血病细胞MEL为研究对象,研究SR48968对三种白血病细胞生长的作用。通过MTT实验和光学显微镜观察发现SR48968对三种白血病细胞均具有剂量和时间依赖的抑制作用,通过Hoechst 33342荧光染色实验发现SR48968抑制白血病细胞的生长有可能是通过诱导凋亡途径所介导,通过双向电泳分析发现SR48968作用前后白血病细胞中产生了一百多个差异蛋白点。本文的研究结果将有助于进一步深入系统研究神经激肽受体与肿瘤发生发展的关系,后续深入系统的研究将对临床肿瘤的诊治工作提供新的思路和潜在的药物。

Previous studies showed that the expression levels of the neurokinin receptos were changed in some tumors or cancer cells. SR48968 is an antagonist of the neurokinin receptor 2. Leukaemia is a type a disease which have serious harm to human health. In this study, the human chronic myelogenous leukemia cells K562, the human acute myeloid leukemia cells HL-60 and the murine erythroleukemia cells MELwere used to investigate the effects of SR48968 to the three leukaemia cells. The results of MTT test and optical microscopy observation showed that SR48968 inhibited the growth of the three types of cells in a dose- and time-dependent manner. Moreover, the inhibited effects of the growth of leukaemia cells induced by SR48968 may be mediated through an apoptosis pathway, which was obtained from the Hoechst 33342 staining test. Additionally, the data from two dimensional electrophoresis(2-DE)showed that the expression levels of more than 100 proteins were changed after administrated SR48968.The results of this study will be helpful to the further study between the neurokinin receptors and the occurrence and development of tumors, and the future follow-up studies in depth will provide new ideas and potential drugs in diagnosis and treatment of clinical tumors.

付彩云、王强、陈攀峰、张世馥、王宇沙、寿鑫、应芊芊

肿瘤学基础医学药学

白血病细胞神经激肽受体2SR48968

kleukaemia cellsneurokinin receptors 2SR48968

付彩云,王强,陈攀峰,张世馥,王宇沙,寿鑫,应芊芊.神经激肽受体2的拮抗剂SR48968对三种白血病细胞的作用及其作用机制的初步探讨[EB/OL].(2011-04-25)[2025-08-18].http://www.paper.edu.cn/releasepaper/content/201104-588.点此复制

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