现代医药卫生
現代醫藥衛生
현대의약위생
MODERN MEDICINE HEALTH
2014年
21期
3206-3208
,共3页
地塞米松%肺肿瘤%腺癌%紫杉酚%抗药性%基因表达%细胞凋亡
地塞米鬆%肺腫瘤%腺癌%紫杉酚%抗藥性%基因錶達%細胞凋亡
지새미송%폐종류%선암%자삼분%항약성%기인표체%세포조망
Dexamethasone%Lung neoplasms%Adenocarcinoma%Paclitaxel%Drug resistance%Gene expres-sion%Apoptosis
目的：观察紫杉醇（PTX）干预不同浓度地塞米松（DEX）预处理人肺腺癌A549细胞后的耐药情况和Bcl-xL基因及蛋白表达变化，探讨DEX诱导A549细胞对PTX产生耐药的分子机制。方法采用四甲基偶氮唑蓝比色法（MTT法）测定不同浓度PTX作用于A549细胞后的细胞存活率，筛选出PTX的半数抑制浓度（IC50）；用不同浓度DEX预处理A549细胞后，再给予不同浓度PTX作用于A549细胞，用MTT法测定细胞存活率，逆转录-聚合酶链反应和蛋白质印迹法检测细胞中Bcl-xL基因和蛋白的表达。结果不同浓度DEX预处理A549细胞后能诱导其对PTX产生耐药，细胞存活率随 DEX 浓度的增加而增高，Bcl-xL 基因和蛋白表达水平随 DEX 浓度的增加而增高。结论 DEX 能诱导A549细胞对PTX产生耐药，其机制可能与DEX诱导A549细胞抗凋亡Bcl-xL基因表达增加有关。
目的：觀察紫杉醇（PTX）榦預不同濃度地塞米鬆（DEX）預處理人肺腺癌A549細胞後的耐藥情況和Bcl-xL基因及蛋白錶達變化，探討DEX誘導A549細胞對PTX產生耐藥的分子機製。方法採用四甲基偶氮唑藍比色法（MTT法）測定不同濃度PTX作用于A549細胞後的細胞存活率，篩選齣PTX的半數抑製濃度（IC50）；用不同濃度DEX預處理A549細胞後，再給予不同濃度PTX作用于A549細胞，用MTT法測定細胞存活率，逆轉錄-聚閤酶鏈反應和蛋白質印跡法檢測細胞中Bcl-xL基因和蛋白的錶達。結果不同濃度DEX預處理A549細胞後能誘導其對PTX產生耐藥，細胞存活率隨 DEX 濃度的增加而增高，Bcl-xL 基因和蛋白錶達水平隨 DEX 濃度的增加而增高。結論 DEX 能誘導A549細胞對PTX產生耐藥，其機製可能與DEX誘導A549細胞抗凋亡Bcl-xL基因錶達增加有關。
목적：관찰자삼순（PTX）간예불동농도지새미송（DEX）예처리인폐선암A549세포후적내약정황화Bcl-xL기인급단백표체변화，탐토DEX유도A549세포대PTX산생내약적분자궤제。방법채용사갑기우담서람비색법（MTT법）측정불동농도PTX작용우A549세포후적세포존활솔，사선출PTX적반수억제농도（IC50）；용불동농도DEX예처리A549세포후，재급여불동농도PTX작용우A549세포，용MTT법측정세포존활솔，역전록-취합매련반응화단백질인적법검측세포중Bcl-xL기인화단백적표체。결과불동농도DEX예처리A549세포후능유도기대PTX산생내약，세포존활솔수 DEX 농도적증가이증고，Bcl-xL 기인화단백표체수평수 DEX 농도적증가이증고。결론 DEX 능유도A549세포대PTX산생내약，기궤제가능여DEX유도A549세포항조망Bcl-xL기인표체증가유관。
Objective To observe the changes of the drug resistance of lung adenocarcinoma A549 cells and the expres-sion of mRNA and protein of Bcl-xL in human lung adenocarcinoma A549 cell after dexamethasone(DEX) pretreatment in dif-ferent concentrations and intervention with paclitaxel(PTX),and to explore the molecular mechanism of DEX-induced A549 cell to the drug resistance of PTX. Methods The cell viability rate of lung adenocarcinoma A549 cells was determined by MTT assay after treatment of different concentrations of PTX,and to screen the half inhibitory concentration(IC50) of PTX. The cell viability rate of A549 cells which pretreated with different concentrations of DEX and different concentrations of PTX was determined by MTT assay,and the expression level of mRNA and protein of Bcl-xL in the A549 cells were determined by reverse transcriptase-poly merase chain reaction(RT-PCR) and Western blotting. Results After being pretreated with DEX in different concentrations, A549 cells were induced to resist to PTX,and the rate of resistance increased gradually with the increasing concentrations of DEX and the expression level of Bcl-xL gene and protein also increased gradually with the increasing of DEX concentrations. Conclu-sions DEX can induce resistance to PTX in lung adenocarcinoma A549 cells ,whose mechanism might be involved in increase of Bcl-xL gene(anti-apoptosis gene) in DEX-induced lung adenocarcinoma A549 cells.
