摘要
目的:探讨当归多糖对K562白血病细胞JAK2、STAT3表达和活化的影响。方法:采用免疫细胞化学和激光共聚焦扫描显微镜观察当归多糖(200mg/L)作用K562细胞不同时间STAT3的表达变化;免疫印迹法检测JAK2、Phospho-STAT3、细胞质和细胞核中STAT3的表达水平。结果:当归多糖作用K562细胞12h,胞核中STAT3表达较对照组明显减少,而胞质内的表达明显增多;当归多糖作用72h,细胞核内STAT3表达比对照组减少,但胞质内的表达差异不显著。免疫印迹法显示12、24、36、48h胞质中STAT3表达增多,STAT3较对照组减少;各时间点STAT3磷酸化水平较对照组降低,JAK2的表达均无显著变化。结论:当归多糖抑制K562细胞增殖,促进其分化、诱导凋亡的机制与其对JAK2/STAT3信号转导分子的表达和核转位活化密切相关。
Objective: To approach the influence of angelica polysaccharide (APS) on the expression and activity of JAK2 and STAT3 in K562 cells, and reveal the molecular mechanism of the regulation of APS on differentiation and apoptosis of K562 cells treated with APS. Methods: The expression of JAK2 and STAT3 in K562 cells induced by APS (200 mg/L) at different time were detected by inununocytochemistry and laser confocal scanning microscope; JAK2, Phospho-STAT3 and STAT3 in nucleus and cytoplasm were measured by western blot in each group at different time. Results: The expression of STAT3 in nucleus of APS group was obviously less than that of the control group at 12 h, but the expression in cytoplasm was opposite;There was no difference of STAT3 expression in cytoplasm between APS group and the control group at 72 h. The expression of STAT3 protein in nucleus was down after treatment with APS for 72 h. The results of western blot showed that the expression of STAT3 in cytoplasm was increased in APS treated cells at 12 h, 24 h, 36 h and 48 h, compared with that of control group. STAT3 protein in nucleus and phosphor-STAT3 was rapidly down in K562 cells induced by APS; whereas the expression level of JAK2 was unchanged. Conclusion: The expression of JAK2/STAT3 plays an important role in the effect of APS on proliferation, differentiation and apoptosis.
出处
《解剖学杂志》
CAS
CSCD
北大核心
2009年第1期8-11,共4页
Chinese Journal of Anatomy
基金
国家自然科学基金(30572429)
关键词
当归多糖
白血病
酪氨酸激酶2
信号转导和转录活化因子3
angelica polysaccharide
leukemia
Janus activation kinases 2
signal transducer and activator of transcription 3