三氧化二砷对人肺腺癌细胞凋亡及LRP、MRP基因表达的影响  

Apoptosis and LRP,MRP Gene Expression Induced by Arsenic Trioxide in lung adenocarcinoma cells

作　　者：林浩[1] 韩冰[2] 洪管秋 

机构地区：[1]浙江省云和县人民医院内科,云和323600 [2]哈尔滨医科大学第一临床医学院呼吸内科,哈尔滨150001

出　　处：《海峡药学》2010年第1期92-94,共3页Strait Pharmaceutical Journal

摘　　要：目的探讨三氧化二砷(As2O3)对人肺腺癌细胞凋亡和LRP、MRP基因表达的影响。方法选用人肺腺癌A549细胞株,运用体外细胞培养法,MTT法,流式细胞术检测As2O3对人肺腺癌的抑制和诱导凋亡作用;用逆转录-聚合酶链反应(RT-PCR)方法检测LRP、MRP mRNA的表达。结果As2O3对人肺腺癌A594细胞具有抑制作用,其抑制率呈时间-剂量依赖关系。不同浓度的As2O3均可诱导凋亡。1.0μmol.L-1、2.0μmol.L-1浓度的As2O3可下调LRP、MRP mRNA的表达。结论As2O3具有诱导人肺腺癌细胞凋亡的作用,其机制与其下调LRP、MRP mRNA的表达密切相关。OBJECTIVE To observe the effects of arsenic trioxide （As2O3） on apoptosis, as well as LRP, MRP gene expression in lung adenocarcinoma ceils. METHODS Human lung adenocarcinoma cell line A549 was cultured in vitro. The anti-proliferation and apoptosis effect of As2O3 on A549 was measured by MTT and flow cytometry; reverse transcription-polymerase chain reaction （RT-PCR） was performed to detect LRP and MRP mRNA expression. RESULTS As2O3 inhibited the proliferation of A594 in a time-and dose-dependent manner, and different concentrations of As2O3 could induce A594 apoptosis. In addition, the concentration of As2O3 with 1.0μmol·L^-1 and 2.0μmol· L^-1 could reduce LRP and MRP mRNA expression. CONCLUSION As2O3 can induce apoptosis of lung adenocarcinoma cells through a mechanism of down-regulation of expressions of LRP and MRP mRNA.

关 键 词：肺腺癌 三氧化二砷 肺耐药蛋白 凋亡 

分 类 号：R969.4[医药卫生—药理学]