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俞 康 吴建波 沈志坚 胡晓霞 郭守芳
摘 要 目的：研究不同Ara-c浓度时白血病细胞凋亡的情况和G-CSF、IL-3+G-CSF对其的拮抗作用。方法：分别用不同剂量Ara-c诱导白血病细胞凋亡，同时加G-CSF、IL-3+G-CSF作为拮抗剂，分G-CSF、IL-3+G-CSF、Ara-c三组。通过形态学、DNA电泳、蛋白电泳免疫印迹法观察白血病细胞的凋亡情况。结果：随着Ara-c剂量的增加，凋亡细胞数增高。G-CSF能拮抗低剂量及常规剂量Ara-c诱导的凋亡，但不能完全拮抗中剂量Ara-c，而IL-3+G-CSF能拮抗中剂量Ara-c。Bcl-2表达蛋白IL-3+G-CSF组高于G-CSF组，G-CSF组高于Ara-c组。结论：IL-3、G-CSF能拮抗Ara-c诱导的白血病细胞凋亡。调节Bcl-2基因的表达是细胞因子拮抗凋亡的机制之一。临床应合理、适时地使用细胞因子。
关键词 凋亡 白细胞介素3 粒细胞集落刺激因子
中国图书分类号 R733.702 R331.1
The inhibitory effect of IL-3, G-CSF on
the apoptosis of leukemia cell induced by Ara-c
YU Kang, WU Jian-Bo, SHEN Zhi-Jian et al.
Department of Hematology of the First Hospital Wenzhou Medical College, Wenzhou 325000
Abstract Objective: To study apoptosis of leukemia cell under vary concentratin of Ara-c and the inhibitory effect of G-CSF,IL-3+G-CSF. Methods: Observed the number of apoptotic cell in leukemia induced by vary concentration of Ara-c in morphology, DNA electrophoresis, immunoblotting. There were three groups: Ara-c, G-CSF and IL-3+G-CSF. Results: The number of apoptotic cell was increased while the dose of Ara-c araised. CSF can inhibit apoptosis by low and regular dose Ara-c, but can not complete inhibit the middle dose Ara-c. IL-3+G-CSF can do it. The protein expressed by Bcl-2 in IL-3+G-CSF group is higher than that in G-CSF group, G-CSF group is lower than Ara-c group. Conclusion: This indicate that IL-3, G-CSF can inhibit apoptosis of leukemia cell induced by Ara-c and regulation of Bcl-2 gene expression is the one of mechanism of cytokine inhibiting apoptosis. The results suggest that cytokine be used reasonably and timely in order to gain more effective chemical treatment.
Key words Apoptosis IL-3 G-CSF
阿糖胞苷(Ara-c)是在髓细胞白血病化疗中广为使用的抗代谢药物，近年研究表明，作用于核酸代谢不同环节的药物均能诱导肿瘤细胞的凋亡，凋亡亦是抗肿瘤药物杀灭肿瘤细胞的重要机制之一，而促细胞生长因子包括白介素3(IL-3)、粒细胞集落生长因子(G-CSF)均有明显抑制凋亡的作用。为探讨更合理地应用化疗药物及细胞生长因子，本文研究了不同浓度的Ara-c诱导新鲜白血病细胞的凋亡及IL-[1] [2] [3] 下一页
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