摘要
目的:研究不同Arac浓度时白血病细胞凋亡的情况和GCSF、IL3+GCSF对其的拮抗作用。方法:分别用不同剂量Arac诱导白血病细胞凋亡,同时加GCSF、IL3+GCSF作为拮抗剂,分GCSF、IL3+GCSF、Arac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Arac剂量的增加,凋亡细胞数增高。GCSF能拮抗低剂量及常规剂量Arac诱导的凋亡,但不能完全拮抗中剂量Arac,而IL3+GCSF能拮抗中剂量Arac。Bcl2表达蛋白IL3+GCSF组高于GCSF组,GCSF组高于Arac组。结论:IL3、GCSF能拮抗Arac诱导的白血病细胞凋亡。调节Bcl2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。
Objective: To study apoptosis of leukemia cell under vary concentration 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.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
1999年第5期217-218,共2页
Chinese Journal of Immunology