人参单体RH2诱导人肺腺癌A549D

人参单体Rh2诱导人肺腺癌A/DDP细胞凋亡的体外研究

周东波　胡成平　苏晓丽　杨红忠

　背景与目的　肺癌已成为人类癌症主要死亡原因之一。从植物中开发抗肿瘤药物是国内外抗肿瘤新药开发的一个热点。本研究的目的是观察人参单体Rh2诱导人肺腺癌A/DDP细胞系凋亡的作用,并探讨其可能的分子机制。方法　体外培养的人肺腺癌A/DDP细胞经不同浓度梯度的人参单体Rh2干预,分别应用MTT实验观察其对细胞增殖的影响,用流式细胞术检测细胞周期、凋亡指数及相关基因表达的改变,以及用双抗体夹心ELISA法测定细胞上清液sApo21/Fas浓度变化。结果　①人参单体Rh2可抑制A/DDP细胞的生长,并呈剂量、时间依赖作用。②人参单体Rh2处理A/DDP细胞24h,实验组凋亡指数显著高于对照组(P0.),G0/G1期细胞比例显著高于对照组(P0.01),S期细胞比例显著低于对照组(P0.01),G2/M期细胞比例与对照组比较无显著性差异(P0.05)。③实验组p53、Fas阳性表达率显著高于对照组(P0.01,P0.),Bcl22阳性表达率显著低于对照组(P0.)。④实验组A/DDP细胞培养上清液于不同时间sApo21/Fas含量均显著低于对照组(P0.05)。结论　人参单体Rh2具有诱导人肺腺癌A/DDP细胞凋亡的作用,其分子机制可能是上调p5和Fas及下调Bcl22的表达、通过Fas/FasL系统途径诱导细胞凋亡。

　人参单体Rh2 　　肺肿瘤 　　A/DDP细胞株 　　凋亡

　R.5;R.2

StudyonapoptosisofhumanlungadenocarcinomacelllineA/DDPinducedbyginsenosideRh2invitro

ZHOUDongbo,HUChengping,SUXiaoli,YANGHongzhong.

DepartmentofRespiratoryMedicine,XiangyaHospital,CentralSouthernUniversity,Changsha,Hunan,P.R.China

Correspondingauthor:HUChengping、

　Backgroundandobjective　Lungcancerisoneoftheleadingcausesofcancer2relateddeathinmankind.Toexploitantitumordrugfromplanthasbeenahighlightathomeandabroad.TheaimofthisstudyistoinvestigatetheapoptosisofhumanlungadenocarcinomacelllineA/DDPinducedbyginsenosideRh2(G-Rh2)andtoexploreitspossiblemolecularmechanism.Methods　ThegrowthinhibitioneffectofG-Rh2onA/DDPcellswasevaluatedbyMTTassay.Cellcycleanalysis,apoptosisindexandtumorrelatedgeneexpressionweredetectedbyflowcytometry.ThechangesofsApo21/FaslevelinthecellculturesupernatantweredeterminedbyELISAmethod.Results　①G-Rh2significantlyinhibitedthegrowthofA/DDPcellsinadosetimedependentmanner.②After24hours’treatmentwithG-Rh2,apoptosisindexoftrialgroupwassignificantlyhigherthanthatofcontrolgroup(P0.).TheproportionofcellsinG0/G1phaseintrialgroupwasmuchhigherthanthatincontrolgroup(P0.01),whileproportioninSphaseintrialgroupwasmarkedlylowerthanthatincontrolgroup(P0.01).TherewasnosignificantdifferenceinproportioninG2/Mphasebetweentrialgroupandcontrolgroup(P0.05).③Thepositiveexpressionrateofp53andFasintrialgroupwassignificantlyhigherthanthatincontrolgroup(P0.01,P0.),whilethepositiveexpressionrateofBcl22intrialgroupwassignificantlylowerthanthatincontrolgroup(P0.).④ThelevelofsApo21/FasinA/DDPcellculturesupernatantintrialgroupwasremarkablylowerthanthatincontrolgroup(P0.05).Conclusion　G-Rh2caninducetheapoptosisofA/DDPcells.Itsmolecularmechanismmaybeupregulatingexpressionofp53andFasanddownregulatingexpressionofBcl22.

GinsenosideRh2(G-Rh2)，Lungneoplasms，A/DDPcell，Apoptosis

肺癌是我国乃至世界发病率最高的恶性肿瘤。随着以铂类为一线药物的方案在晚期非小细胞肺癌化疗中的广泛应用,肺癌对铂类的耐药已成为目前







































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