摘要
目的:本研究为观察rhlL-6对小鼠造血功能的影响。方法:应用致死性(?)Co-Y射线辐照BALB/c小鼠,造成骨髓型放射损伤模型。在照射后用rhIL-6皮内注射给药6天(2pg/Bid/只),通过检测出、凝血时间(BT、CT)、凝血酶原时间(PT)、外周血PLT和WBC,以及骨髓造血细胞体外培养CFU-Mix和脾脏CFU-S的数目,研究rhIL-6对骨髓型放射损伤小鼠早期造血功能恢复的效应,并进行机理的探讨。结果:rhIL-6处理组小鼠的BT、CT和PT均比对照组显著缩短(P<0.01),外周血PLT和WBC分别比对照组提高130％和165％,促进造血干/祖细胞(HSC/HPC)增殖、分化。骨髓造血细胞体外培养CFU-Mix和脾脏CFU-S计数均显著高于对照组(P<0.01)。结论:以上说明rhIL-6具有促进造血干/祖细胞(HSC/HPC)增殖,分化有利于受照小鼠早期造血细胞恢复的生物效应,可减轻辐射所致的骨髓造血功能的损伤。
Purpose:Through the experiment of using the highly expressed rhIL-6 E.coli,and of Sephadex G 50,which gains more than 95% purity and 4. 83×108μ/mg contrast activity,to observe the effects of rhIL-6 on hematopoiesis of murine. -Method :BALB/c mice receved a lethal dose irradiation from 50Co-γto establish a model of acute bone marrow type radiation in-jury. After radiation, subcutaneous injection of rhIL-6 is given to the mice for 6 days (2μg/Bid). By observing changes in BT, CT,PT,peripheral PLT and WBC,CPU-Mix cultured in Vitro and CFU-S in spleen,analysis was thus made on the effects of these rhIL-6 on the recovery from radiationinduced hematopoietic aplasis in order to study its mechanisms. Results:It was shown that the BT.CT and TP of the rhIL-6 treatment group is remarkably shorter than that of the control group (P<0. 01). The pe-ripheral PLT and WBC incerased to 130% and 165%. The CPU-Mix cultured m Vitro and CFU-S are markedly higher than that of the control group (P<0. 01) after H test. Conclusion: This research suggests that rhIL-6 exerts biological effects on the hematopoietic cells of radiation-induced murine, it can attenuate radiation injury and stinulate the proliferation and differentiation of hematopoietic stem/proginitor cells,and help hematopietic recovery of bone marrow.
出处
《临床肿瘤学杂志》
CAS
1997年第1期4-8,共5页
Chinese Clinical Oncology
