癌变·畸变·突变
癌變·畸變·突變
암변·기변·돌변
CARCINOGENSES,TERATOGENSIS AND MUTAGENESIS
2015年
1期
6-10
,共5页
刘锋%陈志添%邵孔健%萨本仲
劉鋒%陳誌添%邵孔健%薩本仲
류봉%진지첨%소공건%살본중
洋地黄毒苷%肺癌%细胞周期调控%细胞周期蛋白A1
洋地黃毒苷%肺癌%細胞週期調控%細胞週期蛋白A1
양지황독감%폐암%세포주기조공%세포주기단백A1
digitoxin%lung cancer%regulation of cell cycle%Cyclin A1
目的：探讨洋地黄毒苷对肺癌NCI-H446与A549细胞增殖和细胞周期的影响，并初步探讨其可能的作用机制。方法：体外培养的NCI-H446与A549细胞分别经不同浓度(10、20、40、80、160 nmol/L)的洋地黄毒苷处理24、48和72 h后，采用MTT法检测细胞增殖情况，应用流式细胞术检测洋地黄毒苷处理细胞48 h后各组细胞周期分布，Western blot检测细胞中Cyclin A和P21蛋白表达水平。结果：与未经洋地黄毒苷处理的对照组相比，不同浓度(10、20、40、80和160 nmol/L)的洋地黄毒苷均可抑制 NCI-H446与A549细胞的增殖，均呈剂量和时间依赖性(P<0.05)，作用48 h后，洋地黄毒苷对NCI-H446与A549细胞的IC50值分别为61.26 nmol/L和110.73 nmol/L。流式细胞仪分析结果显示，随药物作用浓度增加，G0/G1细胞比例降低，S期细胞比例显著增加，与对照组相比，差异具有统计学意义(P<0.05)。Western blot分析结果显示，洋地黄毒苷能剂量依赖性的下调Cyclin A1蛋白表达和上调P21蛋白的表达(P<0.05)。结论：洋地黄毒苷可抑制体外培养的肺癌NCI-H446与A549细胞增殖，诱导细胞发生S期阻滞，其机制可能与细胞周期相关调控蛋白的表达有关。
目的：探討洋地黃毒苷對肺癌NCI-H446與A549細胞增殖和細胞週期的影響，併初步探討其可能的作用機製。方法：體外培養的NCI-H446與A549細胞分彆經不同濃度(10、20、40、80、160 nmol/L)的洋地黃毒苷處理24、48和72 h後，採用MTT法檢測細胞增殖情況，應用流式細胞術檢測洋地黃毒苷處理細胞48 h後各組細胞週期分佈，Western blot檢測細胞中Cyclin A和P21蛋白錶達水平。結果：與未經洋地黃毒苷處理的對照組相比，不同濃度(10、20、40、80和160 nmol/L)的洋地黃毒苷均可抑製 NCI-H446與A549細胞的增殖，均呈劑量和時間依賴性(P<0.05)，作用48 h後，洋地黃毒苷對NCI-H446與A549細胞的IC50值分彆為61.26 nmol/L和110.73 nmol/L。流式細胞儀分析結果顯示，隨藥物作用濃度增加，G0/G1細胞比例降低，S期細胞比例顯著增加，與對照組相比，差異具有統計學意義(P<0.05)。Western blot分析結果顯示，洋地黃毒苷能劑量依賴性的下調Cyclin A1蛋白錶達和上調P21蛋白的錶達(P<0.05)。結論：洋地黃毒苷可抑製體外培養的肺癌NCI-H446與A549細胞增殖，誘導細胞髮生S期阻滯，其機製可能與細胞週期相關調控蛋白的錶達有關。
목적：탐토양지황독감대폐암NCI-H446여A549세포증식화세포주기적영향，병초보탐토기가능적작용궤제。방법：체외배양적NCI-H446여A549세포분별경불동농도(10、20、40、80、160 nmol/L)적양지황독감처리24、48화72 h후，채용MTT법검측세포증식정황，응용류식세포술검측양지황독감처리세포48 h후각조세포주기분포，Western blot검측세포중Cyclin A화P21단백표체수평。결과：여미경양지황독감처리적대조조상비，불동농도(10、20、40、80화160 nmol/L)적양지황독감균가억제 NCI-H446여A549세포적증식，균정제량화시간의뢰성(P<0.05)，작용48 h후，양지황독감대NCI-H446여A549세포적IC50치분별위61.26 nmol/L화110.73 nmol/L。류식세포의분석결과현시，수약물작용농도증가，G0/G1세포비례강저，S기세포비례현저증가，여대조조상비，차이구유통계학의의(P<0.05)。Western blot분석결과현시，양지황독감능제량의뢰성적하조Cyclin A1단백표체화상조P21단백적표체(P<0.05)。결론：양지황독감가억제체외배양적폐암NCI-H446여A549세포증식，유도세포발생S기조체，기궤제가능여세포주기상관조공단백적표체유관。
OBJECTIVE:To investigate the effects of digitoxin on proliferation and cell cycle of human lung cancer cell lines NCI-H446 and A549,and to explore its possible mechanisms.METHODS:NCI-H446 and A549 cells were treated with digitoxin at different concentrations(10,20,40,80 and 160 nmol/L). The effect on proliferation of NCI-H446 and A549 cells were detected by MTT assay. Flow cytometry was used to test the cell cycle distribution of NCI-H446 and A549 cells. Protein expressions of Cyclin A1 and P21 in NCI-H446 and A549 cells were evaluated by Western blot.RESULTS:As compared with control group,cell proliferation was inhibited by digitoxin in a dose- and time-dependent manner(P<0.05),the IC50 value for digotoxin were 61.26 nmol/L in NCI-H446 and 110.73 nmol/L in A549 at 48 h. After 48 h treatment,the proportion of NCI-H446 and A549 cells in G0/G1 phase was decreased,while the proportion in S phase was increased. Western blot analysis showed that digitoxin could significantly up-regulate the expression of Cyclin A1 and down-regulate the expression of P21 in a dose-dependent way(P<0.05).CONCLUSION: Digitoxin could exert an the anti-proliferative effect on NCI-H446 and A549 cells and induce S phase arrest in vitro. The mechanism may be related to the expressions of proteins associated with cell cycle.
