高乌甲素对非小细胞肺癌体外杀伤作用及其分子机制  

Cytotoxic Effect of Lappaconitine on Non-small Cell Lung Cancer in vitro and Its Molecular Mechanism

作　　者：盛良翮[1] 徐萌[1] 徐立群[2] 熊斐[3] 

机构地区：[1]广州暨南大学附属第一医院肿瘤科,广东广州510632 [2]广州医科大学附属肿瘤医院,广东广州510095 [3]中山大学附属第六医院,广东广州510655

出　　处：《中药材》2014年第5期840-843,共4页Journal of Chinese Medicinal Materials

基　　金：国家自然科学基金项目(81273814)

摘　　要：目的:探讨高乌甲素对人非小细胞肺癌A549细胞株增殖、凋亡、细胞周期的影响及其可能机制。方法:体外培养人非小细胞肺癌细胞株A549细胞,以不同浓度高乌甲素干预,采用MTT法、流式细胞术、实时荧光定量PCR法检测等技术,研究不同浓度高乌甲素对其增生、凋亡、细胞周期及Cyclin E1 mRNA表达的影响。结果:高乌甲素可呈剂量依赖性抑制A549细胞增殖。随着高乌甲素浓度的增加,A549细胞G1+G0期细胞所占比例逐渐上升,而S期和G2+M期所占比例逐渐下降;凋亡率逐渐升高,同时Cyclin E1表达下调。结论:高乌甲素具有抗肿瘤作用,其机制可能与诱导肿瘤细胞凋亡、细胞周期阻滞,下调Cyclin E1表达有关。Objective：To evaluate the proliferation inhibitory effect of Lappaconitine（LAP） on non-small cell lung cancer cell line A549 cells in vitro and its possible mechanism. Methods ： A549 cell was euhured with different concentrations of LAP. Cellular prolifera- tion was determined with MTT. Cell cycle and apoptosis were detected with FCM technology. The Cyclin El geue expression was eheeked by Real-time Quantitative PCR method. Results ： LAP could inhibit the proliferation of A549 cells in vitro in a dose-dependent manner. LAP could induce apoptosis of A549 cell. Cell cycle was stopped at the GI ＋ GO phase by LAP with FCM technology. With the increasement of LAP concentration, the ratio of G~ ＋ GO phase was increased and the ratio of S phase and G2 ＋ M phase was decreased ; The apoptotie rate was gradually increased, and the Cyclin E1 gene expression was down-regulated. Conclusion：LAP has the inhibitory effect on the growth of A549 cells ,which is related to the cell cycle arrest in G0/G1 phase ,apoptosis and down-regulation of Cyclin E1 gene expression.

关 键 词：高乌甲素 非小细胞肺癌 A549细胞 细胞周期 凋亡 

分 类 号：R285.5[医药卫生—中药学]