冬凌草甲素诱导GBC-SD细胞凋亡及对bcl-2,p53,fas/apo-1和c-myc表达的影响  

Effect of rubescensine A on apoptosis and bcl-2,p53,fas/apo-1 and c-myc expression in GBC-SD cells

作　　者：薛宏伟[1] 潘祥麟[1] 杨尚军[2] 

机构地区：[1]山东大学第二医院血液肿瘤科,山东济南250033 [2]山东省医学科学院药物研究所,山东济南250012

出　　处：《山东大学学报（医学版）》2005年第4期336-339,共4页Journal of Shandong University:Health Sciences

摘　　要：目的:探讨冬凌草甲素(RuA)对人胆囊癌细胞株(GBC-SD)诱导凋亡的机制。方法:用不同浓度的RuA处理GBC-SD细胞,MTT法检测RuA对GBC-SD细胞生长的抑制作用,通过倒置显微镜、扫描电子显微镜、流式细胞术、荧光分光光度法观察凋亡细胞的形态结构变化,定量检测细胞凋亡及半胱天冬酶(caspase-3)的活性,免疫组化法检测核磷蛋白p53、bcl-2蛋白、fas/apo-1及c-myc蛋白的表达。结果:RuA能诱导细胞凋亡,并呈浓度依赖性。药物作用24h后,对照组和实验组细胞中bcl-2,p53,fas/apo-1和c-myc蛋白的表达差异具有统计学意义(P<0.05)。结论:RuA诱导GBC-SD细胞凋亡与bcl-2,p53,fas/apo-1和c-myc的表达有关。Objective: To investigate the mechanism of GBC-SD(gallbladder cell-Shandong) apoptosis induced by Rubescensine A. Methods: The presence and pathogenesis of apoptosis were demonstrated by the method of MTT, convert microscopy, electron microscopy, flow cytometry, immunohistochemical assay and spectrofluorometry. Results: After exposure to Rubecensine A , GBC-SD cells were induced to apoptosis in dose-dependent manner, and the level of bcl-2, p53, c-myc and fas/apo-1 were decreased within 24 hours, but the activity of caspase-3 was enhanced with the appearance of apoptosis. Conclusion: Rubescensine A can induce the inhibition of cell growth by apoptosis related to bcl-2, p53, fas/apo-1 and c-myc.

关 键 词：冬凌草甲素 细胞凋亡 人胆囊癌细胞系 

分 类 号：R735.8[医药卫生—肿瘤]