摘要
目的分析丁酸钠(SB)诱导 NB4细胞凋亡后细胞蛋白质组的变化,以探讨 SB 诱导NB4细胞凋亡的分子机制。方法在 NB4细胞培养体系中,加入1.0 mmol/LSB,用流式细胞术检测对照组及加药后0,12,24,48,72 h 细胞的凋亡情况;分别取对照组及用药后上述时间点的细胞进行双向凝胶电泳(2-DE),分析不同时间点蛋白质组的变化,用基质辅助激光解析电离飞行时间质谱(MALDI-TOF-MS)和电喷雾串联质潜(ESI-MS/MS)对发生变化的蛋白质进行鉴定分析。结果 SB 可诱导 NB4细胞凋亡,并呈时间依赖性。SB 作用 NB4细胞后21种蛋白发生了明显的变化,这些敏感生白涉及凋亡信号传导、免疫调节、转录调控、细胞代谢、细胞内分子转运等众多细胞内事件。其中13种蛋白已有报道与凋亡相关。结论 SB 不仅可促进肿瘤细胞凋亡,而且可能有增强细胞对化疗药物敏感性及免疫调节作用,新蛋白的鉴定为进一步分析 SB 抗肿瘤作用的机制及筛选新的药物靶点奠定了分子基础。
Objective To explore the molecular mechanisms of apoptotic NB4 cells induced by the histone deacetylase inhibitor, sodium butyrate（SB）. Methods SB was exposed to NB4 ceils at a final concentration of 1.0 mmol/L. The untreated and treated ceils were analysed with FACS and 2-dimentional electrophoresis （2-DE） at 0, 12, 24, 48 and 72 h. The changed protein spots were identified with MALDI-TOF-MS and ESI-TOF-MS/MS. Results SB induced apoptosis of NB4 ceils. Twenty-one changed proteins involving apoptotic signal transduction, immunological regulation, transcriptional control, cellular metabolism, molecular transport and so on were identified. Thirteen of them had been reported to be related to apoptosis. Conclusion SB can induce apoptosis and many functional protein changes in tumor ceils. These results pave the way to further explore the anti-tumor mechanism of SB.
出处
《中华血液学杂志》
CAS
CSCD
北大核心
2006年第7期436-440,共5页
Chinese Journal of Hematology
基金
吉林省计委资助项目(20031268)
