trail联合pdtc对sgc-7901细胞生长抑制和凋亡诱导的实验研究

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1、TRAIL联合PDTC对SGC-7901细胞生长抑制和凋亡诱导的实验研究【摘要】目的观察肿瘤坏死因子相关凋亡诱导配体（TRAIL）及TRAIL联合核转录因子核因子-κB（NF-κB）活性特异性抑制剂吡咯烷二硫代氨基甲酸盐(PDTC)对胃癌细胞SGC-7901的生长抑制和凋亡诱导作用，并寻找逆转TRAIL耐药的方法。方法采用不同浓度的TRAIL及TRAIL联合PDTC作用于胃癌细胞后，MTT法检测细胞生长抑制率，流式细胞仪检测细胞的凋亡率，免疫细胞化学染色方法观察药物作用前后NF-κB表达情况。结果单独使用TRAIL时，随着浓度从50μg/L增加到

2、500μg/L，细胞的生长抑制率和凋亡率逐渐增加（P<0.05）,但这种作用是非线性的。TRAIL联合0.05μmol/L、0.1μmol/LPDTC后肿瘤细胞的生长抑制率和凋亡率较单用TRAIL显著下降（P<0.05）；而联合1μmol/L、10μmol/LPDTC后其作用较上有所上升（P<0.05）。联合作用组p65蛋白在胞核中染色的强度低于单纯使用TRAIL组（P<0.05）。结论TRAIL对胃癌细胞株SGC-7901具有一定程度的生长抑制和凋亡诱导作用；NF-κB信号转导途径可能具有双向调节作用，大剂量PDTC可能

3、逆转胃癌细胞对TRAIL的耐药。【关键词】肿瘤坏死因子相关凋亡诱导配体；吡咯烷二硫代氨基甲酸盐；胃癌细胞；凋亡；核因子-κB12Abstract：ObjectiveToobservetheeffectofacombinationofpyrrolidinedithiocarbonate(PDTC),aspecificinhibitorofNF-κBandtumornecrosisfactor(TNF)-relatedapoptosis-inducingligand(TRAIL)ontheapoptosisofgastriccancercellsan

4、dtheireffectontheexpressionofNF-κB,andtosearchfortheapproachestoreversingresistancetoTRAILinhumanstomachcancercells.MethodsVariousconcentrationsofTRAILandPDTCwereaddedinexponentialgrowthSGC-7901gastriccancercells.MTTassayswereusedtomeasurethegrowthinhibitoryeffectofcombinedus

5、eofTRAILandPDTCoralone.ApoptosisofgastriccancercellSGC-7901wasanalyzedwithPIstainingmethodandflowcytometry(FCM).TheexpressionofNF-κBwasobservedusingimmunohistochemicalstainingmethod.ResultsAftertheSGC-7901gastriccancercellswereexposedtoTRAILatadoseof50μg/Lto500μg/L,thegrowthi

6、nhibitoryrateandapoptosisrateincreased(P<0.05),buttherewasnolinearityforthisdose-effectrelationship.FollowingTRAILtreatmentincombinationwith0.05μmol/Land0.1μmol/LPDTC,thegrowthinhibitoryrateofandapoptosisratesignificantlydecreasedcomparedwithtreatmentwithTRAILorPDTCalone(P

7、<0.05),whilefollowingTRAILtreatmentincombinationwithPDTC1μmol/Land10μmol/L,thegrowth12inhibitoryrateandapoptosisratesincreasedcomparedwithtreatmentwithTRAILorPDTCalone(P<0.05).ThetwodrugspresentedsynergisticoraddedeffectonSGC-7901cells.TheexpressionofNF-κBdecreasedsubse

8、quenttothetreatmentofPDTC(P<0.05).ConclusionTRAILhastheeffectofgr