摘要
目的 :研究地塞米松 (Dexamethasone ,DEX)诱导人骨髓瘤细胞系Sko 0 0 7凋亡的分子机制及IL 6对此凋亡作用的抑制效应。方法 :MTT法观察DEX对Sko 0 0 7细胞生长的影响 ;碘化丙腚 (propidiumiodide ,PI)染色和流式细胞术分析Sko 0 0 7细胞经DEX处理后的凋亡情况 ;免疫印迹法检测Bcl 2家族抗凋亡蛋白———Bcl 2、Bcl XL 和Mcl 1在Sko 0 0 7细胞凋亡过程中的表达情况。结果 :DEX能够抑制Sko 0 0 7细胞增殖并诱导其发生凋亡 ;同时促进胞内Bcl 2降解。IL 6抑制DEX诱导的Sko 0 0 7细胞凋亡 ,并使Bcl 2表达水平恢复。结论 :IL 6可通过调节Bcl 2表达而实现其对DEX诱导的骨髓瘤细胞凋亡的抑制作用。
Objective:To investigate the mechanism of dexamethasone(DEX) induced apoptosis of human myeloma cell line Sko 007 and the inhibitory effect of IL 6 on apoptosis.Methods:Effect of DEX on the growth of Sko 007 cells was measured by MTT assay;Apoptosis of Sko 007 cells induced by DEX was determined by flow cytometry with propidium iodide(PI) staining of nuclei;The expression of three anti apoptotic Bcl 2 family proteins Bcl 2,Bcl X L and Mcl 1 in Sko 007 cells with or without DEX were determined by immunblot assay.Results:DEX inhibited the proliferation of Sko 007 cells and induced a significant cell apoptosis.In addition,degradation of Bcl 2 can be observed in Sko 007 cells in the presence of Dex.IL 6 stimulation prevented down regulation of Bcl 2 and the apoptosis of Sko 007 cells induced by DEX.Conclusion:IL 6 inhibits DEX induced apoptosis of Sko 007 cells through the specific regulation of Bcl 2.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2002年第11期757-759,共3页
Chinese Journal of Immunology
基金
国家杰出青年科学基金项目 (No3 992 5 0 19)
