TSA对人肝癌细胞SMMC-7721的抑制作用及其机制

目的:研究去乙酰化转移酶抑制剂TSA对肝癌细胞SMMC-7721的作用及其机理。方法:利用细胞计数,流式细胞仪分析细胞凋亡及细胞周期,Tunel试验研究TSA对肝癌细胞SMMC-7721的作用;利用western研究TSA对肝癌细胞蛋白表达的影响。结果:TSA可明显抑制肝癌细胞SMMC-7721的生长,并可诱导细胞凋亡。可阻滞肝癌细胞SMMC-7721细胞周期于G0/G1期。可增加p53,p21,bax等基因的表达,降低BCL-2的表达。结论:去乙酰化转移酶抑制剂TSA可明显抑制肝癌细胞SMMC-7721的生长并诱导其凋亡,其主要通过调控一些肿瘤相关基因的表达起作用。     

鱼藤素对肝癌细胞株SMMC-7721增殖抑制和凋亡诱导作用的研究

目的 研究鱼藤素对肝癌细胞株SMMC-7721增殖和凋亡的影响及其作用机制.方法 MTT法检测鱼藤素对SMMC-7721细胞增殖的抑制作用;DNA琼脂糖凝胶电泳观测细胞凋亡情况;采用Western blotting法检测相关蛋白表达水平的变化,探讨其作用机制.结果 鱼藤素呈剂量和时间依赖性抑制SMMC-7721细胞增殖,诱导细胞凋亡致DNA ladder形成,出现相应的形态学改变;鱼藤素可明显降低Akt的磷酸化水平.结论 鱼藤素可通过下调Akt的活性,抑制SMMC-7721的增殖并诱导细胞凋亡,或可成为一种新的抗肝癌药物.     

AZT对肝癌细胞端粒酶活性及相关蛋白表达的影响

背景与目的：端粒酶抑制剂抑制端粒酶活性的机制十分复杂,可能涉及多个蛋白的共同作用。本研究通过3’-叠氮脱氧胸苷（3’-azido-deoxythymidine,AZT）作用于人肝癌细胞SMMC-7721。比较AZT作用后癌细胞端粒酶活性及相关蛋白的变化,探讨AZT抑制端粒酶活性的可能机制。方法：利用噻唑蓝[3（4,5-demethyhhiazole-2-y1）-2,5-diphenyl tetrazolium-bromide,MTT]实验确定AZT作用的最佳作用时间和浓度;实时荧光定量端粒重复序列扩增法（real-time fluorescent quantitative TRAP assay,FQ-TRAP法）检测AZT作用后,SMMC-7721细胞端粒酶活性变化;用缺口末端标记技术（terminal deoxyribonucleotidyl transferse（TdT）-mediated biotin-16-dUTP nick-end labelling,TUNEL）法和流式细胞术检测AZT作用后．SMMC-7721细胞凋亡情况;单细胞激光拉曼光谱技术和蛋白质芯片-飞行时间质谱仪,检测AZT作用后特异蛋白质的变化。结果：AZT抑制癌细胞生长的最佳作用时间为48h,最佳作用浓度为20mmol／L;FQ-TRAP法检测发现,AZT作用后肝癌细胞端粒酶活性与对照组相比受到明显抑制（P=0．0001）;TUNEL法观察到AZT诱导肝癌细胞凋亡形态学改变．流式细胞术检测AZT诱导肝癌细胞凋亡率为13．5％：单细胞激光拉曼光谱技术观察到,AZT作用后有7个与蛋白代谢相关的特征峰变化;蛋白质芯片．飞行时间质谱仪检测发现,AZT作用后有24个蛋白分子在癌细胞中高表达,8个蛋白分子在癌细胞中低表达,32个差异蛋白均属于小分子蛋白。结论：AZT可抑制SMMC-7721细胞端粒酶活性,诱导凋亡与相关特异小分子蛋白有关。     

Differential sensitivity of human mammary epithelial and breast carcinoma cell lines to curcumin

Curcumin has anti-inflammatory, antiproliferative, and antitumor effects. To understand the chemopreventive mechanism of curcumin against human malignancies, the cellular and molecular changes induced by this agent in human mammary epithelial (MCF-10A) and breast carcinoma (MCF- 7/TH) cell lines were investigated. The human multidrug- resistant breast cancer cell line was 3.5 fold more sensitive to curcumin than the mammary epithelial cell line. Even though both cell lines accumulated a similar amount of curcumin, a significantly higher percentage of apoptotic cells was induced in breast cancer cells compared to a very low percentage of apoptosis in mammary epithelial cells. Incubation of breast cancer cells with 20 and 40 microM curcumin for 24 h induced G2 block and sub-G0/G1 cell population, respectively. Curcumin treatment caused a reduction in the expression of Ki67, PCNA, and p53 mRNAs in breast cancer cells. The human mammary epithelial cell line showed a down-regulation of p21 mRNA and an up-regulation of Bax mRNA expression with curcumin treatment. The results suggest that apoptosis is involved in the curcumin-induced inhibition of tumor cell growth, and genes associated with cell proliferation and apoptosis may be playing a role in the chemopreventive action of curcumin.     

反义DNA甲基转移酶1改变肝癌SMMC-7721细胞对肿瘤坏死因子相关凋亡诱导配体的敏感性及其机理的研究

目的　观察转入反义DNA甲基转移酶 1(DNMT1)基因片段后的肝癌SMMC 772 1细胞对肿瘤坏死因子相关凋亡诱导配体 (TRAIL)的敏感性改变 ,初步阐明其机理。方法　台盼蓝排斥实验检测活细胞率 ;TUNEL法检测细胞凋亡率 ;流式细胞仪检测bcl 2、bax和bad蛋白的表达。结果　转入反义DNMT1基因片段的肝癌SMMC 772 1细胞与转入正义DNMT1基因片段和空载体的细胞相比 ,活细胞率显著降低 (P <0 .0 5,P <0 .0 1) ,凋亡率显著增高 (P <0 .0 5,P <0 .0 1)。流式细胞仪结果显示 ,转入反义DNMT1基因片段的SMMC 772 1细胞 ,其bax和bad表达 ,尤其是bax的表达 ,明显高于转入正义DNMT1基因片段和空载体的细胞 ,但对bcl 2的表达无影响。结论　转入反义DNMT1基因片段的肝癌SMMC 772 1细胞对TRAIL的敏感性明显增强 ,可能与bax和bad的表达增强有关     

塞来昔布抑制肝癌细胞株增殖及其机制的实验研究

目的:研究特异性环氧化酶-2(COX-2)抑制剂塞来昔布对人肝癌细胞株SMMC-7721是否有抑制增殖、诱导凋亡作用并初步探讨其作用机制。方法:采用四氮唑盐比色法(MTT法)观察不同浓度的塞来昔布作用后细胞增殖活力改变;流式细胞仪检测细胞凋亡百分率及细胞周期变化;免疫组化观察Bcl-2蛋白和Bax蛋白表达情况。结果:MTT法显示随着塞来昔布浓度和作用时间增加,细胞增殖抑制率上升;流式细胞仪测定空白对照组未见明显凋亡峰,塞来昔布组出现凋亡峰,凋亡率随着时间及药物浓度变化而变化,二者呈正相关;免疫组化显示经塞来昔布干预后,凋亡蛋白Bax表达增加,而Bcl-2表达减少,并随时间和药物浓度变化而明显。结论:塞来昔布抑制SMMC-7721细胞增殖,促进SMMC-7721细胞凋亡,并呈剂量和时间依赖性。其作用机制之一可能是通过减少Bcl-2的表达,增加Bax的表达,从而启动细胞凋亡途径。     

Iso-suillin Isolated from Suillus luteus,Induces G1 Phase Arrest and Apoptosis in Human Hepatoma SMMC-7721 Cells

Iso-suillin, a natural product isolated from Suillus luteus, has been shown to inhibit the growth of somecancer cell lines. However, the molecular mechanisms of action of this compound are poorly understood. Thepurpose of this study was to investigate how iso-suillin inhibits proliferation and induces apoptosis in a humanhepatoma cell line (SMMC-7721). We demonstrated the effects of iso-suillin on cell proliferation and apoptosisin SMMC-7721 cells, with no apparent toxicity in normal human lymphocytes, using colony formation assaysand 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) analysis. Western blotting was usedto examine the expression of G1 phase-regulated and apoptosis-associated protein levels in iso-suillin treatedSMMC-7721 cells. The results indicated that iso-suillin significantly decreased viability, induced G1 phase arrestand triggered apoptosis in SMMC-7721cells. Taken together, these results suggest the potential of iso-suillin asa candidate for liver cancer treatment.     

冬凌草甲素抑制人肝癌SMMC．7721细胞增殖及诱导细胞凋亡的机制研究

目的研究冬凌草甲素对人肝癌细胞株SMMC-7721细胞的抑制作用及诱导凋亡机制。方法采用不同浓度的冬凌草甲素作用于人肝癌SMMC-7721细胞,以四甲基偶氮唑蓝（MTT）法检测细胞抑制率,倒置显微镜观察不同浓度组的细胞形态,RT—PCR法检测细胞Survivin、Bcl-2、BaxmRNA的表达,WesternBlot法检测细胞Survivin、Bcl-2、Bax的蛋白表达。结果MTT比色法显示不同浓度的冬凌草甲素可抑制人肝癌SMMC．7721细胞的增殖,抑制作用呈时间和剂量依赖性。冬凌草甲素作用48h后细胞表现出特异性凋亡。RT—PCR法和WesternBlot法显示,人肝癌SMMC-7721细胞的BaxmRNA和Bax蛋白随冬凌草甲素浓度增加而表达增加,Bcl-2、SurvivinmRNA和Bcl-2、Survivin蛋白随药物浓度增加而表达下降。结论冬凌草甲素能抑制人肝癌SMMC-7721细胞的生长及诱导细胞发生凋亡,降低Sur—vivin、Bcl-2表达和上调Bax表达可能是诱导细胞发生凋亡的机制。     

水飞蓟宾对人肝癌细胞SMMC-7721体外增殖的影响

目的:探讨水飞蓟宾对SMMC-7721细胞的抗增殖作用。方法:MTT法观察对细胞的抑制作用;免疫细胞化学法检测增殖细胞核抗原(PCNA)及Ki-67的表达;流式细胞仪分析细胞周期及凋亡;光镜及透射电镜观察细胞形态学的变化。结果:水飞蓟宾可抑制SMMC-7721的增殖,并降低PCNA、Ki-67的表达及引起细胞G2/M期阻滞,同时诱导凋亡。光镜发现细胞体积缩小,核固缩深染;电镜可见凋亡及凋亡小体。结论:在体外,水飞蓟宾可抑制SMMC-7721细胞的增殖。     

珠子参体外诱导人肝癌细胞凋亡效应及机制研究

目的观察珠子参体外诱导人肝癌细胞凋亡效应并初探其分子机制。方法体外细胞培养采用人肝癌细胞株SMMC-7721,分为对照(BL)组、珠子参(PJ)组、二甲基亚砜(DMSO)组及5-FU组,采用电镜观察作用后肝癌细胞超微结构改变;流式细胞仪检测肝癌细胞周期和凋亡率;RT-PCR法检测癌基因c-myc、c-fos和抑癌基因p53、p21表达的变化。结果与对照组比较,电镜下珠子参组SMMC-7721细胞染色质浓缩,分解成大小不一有膜包绕团块,内含有新月形DNA物质及细胞器,形成凋亡小体;周期分析可见G0/G1期细胞阻滞,阻止了细胞向S期的转换,并引起细胞凋亡,凋亡率达38.34%;RT-PCR半定量分析珠子参能降低癌基因c-myc表达(P<0.05),增高抑癌基因p53和p21表达(P<0.05)。结论珠子参能诱导人肝癌细胞SMMC-7721凋亡,部分作用机制可能与阻滞细胞停留在G0/G1,降低癌基因c-myc和c-fos表达,增高抑癌基因p53和p21表达有关。     

Anti-hepatoma cells function of luteolin through inducing apoptosis and cell cycle arrest

The aim of this study is to explore the apoptotic induction and cell cycle arrest function of luteolin on the liver cancer cells and the related mechanism. The liver cancer cell line SMMC-7721, BEL-7402, and normal liver cells HL-7702 were treated with different concentrations of luteolin. Cell proliferation ability was tested. Morphological changes of the apoptotic cells were observed under inverted fluorescence microscope after Hoechst33342 staining. We investigated the effect of luteolin on cell cycling and apoptosis with flow cytometry. The mitochondrial membrane potential changes were analyzed after JC-1 staining. Caspases-3 and Bcl-2 family proteins expression were analyzed by real-time PCR. Cell proliferation of SMMC-7721 and BEL-7402 were inhibited by luteolin, and the inhibition was dose–time-dependent. Luteolin could arrest the cells at G1/S stage, reduce mitochondrial membrane potential, and induce higher apoptosis rate and the typical apoptotic morphological changes of the liver carcinoma cells. Q-RT-PCR results also showed that luteolin increased Bax and caspase-3 expression significantly and upregulated Bcl-2 expression in a dose-dependent manner in liver carcinoma cells. However, the normal liver cells HL-7702 was almost not affected by luteolin treatment. Luteolin can inhibit SMMC-7721 and BEL-7402 cell proliferation in a time- and dose-dependent manner. And the mechanism maybe through arresting cell cycle at phase G1/S, enhancing Bax level, reducing anti-apoptotic protein Bcl-2 level, resulting in activating caspase-3 enzyme and decrease of mitochondrial membrane potential, and finally leading to cell apoptosis.     

Celecoxib联合羟基喜树碱对缺氧诱导的人肝癌细胞增殖与凋亡的影响

目的:探讨选择性环氧合酶-2(COX-2)抑制剂Celecoxib联合羟基喜树碱对缺氧诱导的人肝癌细胞株SMMC-7721细胞增殖和凋亡的影响。方法:应用三气培养箱在缺氧环境下培养人肝癌细胞株SMMC-7721细胞。预实验筛选Celecoxib、羟基喜树碱最小有效终浓度,设24、48、72小时为干预时间并筛选最佳作用时间。分别以Celecoxib及羟基喜树碱单独实验筛选的最小有效浓度为联合组浓度;以Celecoxib单独实验筛选最佳作用时间为实验时间。倒置显微镜观察细胞形态学变化;应用四氮唑盐比色法(MTT法)监测细胞增殖活力;Annexin V/PI双染色法检测细胞凋亡;免疫细胞化学法（SP法）检测凋亡蛋白Bax、Bcl-2、COX-2的表达。结果:不同浓度Celecoxib及不同时间对SMMC-7721细胞表现出的生长抑制作用呈剂量依赖性及时间依赖性。Celecoxib（30 mg/L)单用在作用72 h时即可抑制SMMC-7721细胞的增殖。选72 h为作用时间,不同浓度羟基喜树碱对SMMC-7721细胞表现出的生长抑制作用呈剂量依赖性,浓度为0.625 μmol/L羟基喜树碱即可抑制SMMC-7721细胞的增殖。选用羟基喜树碱(0.625 μmol/L)与Celecoxib（30 mg/L)联合作用72 h时,联合抑制作用结果呈现协同作用(Q>1.15)。流式细胞仪检测分析,两种药物均可有效诱导 SMMC-7721细胞的凋亡,并且在上述浓度联合作用时具有协同效应。免疫细胞化学结果显示,Celecoxib（30 mg/L)组和联合用药组细胞质内棕黄色颗粒较对照组染色浅,表明Bcl-2和COX-2蛋白表达有所下降,而Bax蛋白表达在Celecoxib（30 mg/L)和联合用药组中黄色颗粒的阳性细胞较对照组增多,表明Bax蛋白表达有所上调;并且此变化与Celecoxib（30 mg/L)组比较联合用药组有协同作用(P<0.05)。结论:缺氧状态下Celecoxib与羟基喜树碱对SMMC-7721细胞株均有抑制增殖与促进凋亡作用,并且两者联合作用有协同作用;Celecoxib的作用机制除了抑制COX-2外,还可能与下调Bcl-2、上调Bax的表达有关。     

黄芩素诱导人肝癌细胞株SMMC-7721凋亡作用的研究

目的:研究12-脂氧合酶(12-lipoxygenase,12-LOX)在人肝癌细胞株SMMC-7721中的表达,以及选择性12-LOX抑制剂黄芩素对人肝癌细胞SMMC-7721生长、凋亡的影响.方法:采用免疫细胞化学染色及RT-PCR检测12-LOX的蛋白质和mRNA在SMMC-7721中的表达.应用MTT、流式细胞术及TUNEL检测细胞生长及凋亡.蛋白印迹法检测分析Caspase-3,Bcl-2,Bax,phospho-ERK1/2,ERK1/2和β-actin蛋白质的表达.结果:免疫细胞化学技术显示12-LOX蛋白表达于SMMC-7721细胞质.RT-PCR检测到黄芩素呈浓度-时间依赖性地抑制12-LOX mRNA表达.采用黄芩素小同浓度或不同时间段干预细胞SMMC-7721,MTT法检测细胞增殖呈剂量、时问依赖性的下降.原位末端转移酶标记技术及流式细胞仪分析证实12-LOX抑制剂诱导细胞凋亡.蛋白印迹法检测显示,黄芩素干预后,Bcl-2蛋白表达明显下降和Bax蛋白轻微上升,细胞凋亡蛋白酶-3活性水平与黄芩素浓度正相关,黄芩素对细胞凋亡相关蛋白的影响被12 (S)-HETE逆转,12(5)-HETE可能激活ERK1/2磷酸化.结论:人肝癌细胞株SMMC-7721存在12-LOX的表达,12-LOX抑制剂黄芩素可抑制细胞生长和诱导细胞凋亡.     

Survivin反义寡核苷酸对肝癌细胞增殖和凋亡的影响

目的:观察Survivin反义寡核苷酸对SMMC-7721细胞增殖、凋亡的影响。方法:设计合成特异性Survivin反义寡核苷酸,转染肝癌SMMC-7721细胞,MTT法测定Survivin ASODN对细胞增殖抑制情况的影响,FCM法检测对细胞周期、凋亡及Survivin蛋白表达的影响。结果:Survivin ASODN可抑制SMMC-7721细胞的生长增殖,并呈浓度和时间依赖性。ASODN转染组可诱导SMMC-7721细胞凋亡(P<0.01),细胞周期阻滞于G2/M期(P<0.05)。ASODN转染组Survivin蛋白表达水平显著降低(P<0.01)。结论:Survivin ASODN能下调SMMC-7721细胞Survivin表达,并可抑制其增殖并诱导凋亡。     

白眉蝮蛇去整合素rAdinbitor对人肝癌细胞系SMMC-7721细胞黏附与增殖的抑制作用

Objective:To investigate the effects of rAdinbitor on the adhesion and proliferation of human hepatoma cell strain SMMC-7721.Methods:Cell adhesion assay was used to observe the effect of rAdinbitor on the adhesion of SMMC-7721 cells to fibronectin (FN).Crystal violet staining was performed to detect the influence of rAdinbitor on the adhesion of SMMC7721 cells.MTT assay was employed to detect the inhibitory effects of different concentration of rAdinbitor on the proliferation of SMMC-7721 cells.The morphologic changes of the control SMMC-7721 cells and the apoptotic cells induced by 200 μg/mL rAdinbitor for 36 h were observed under light microscope after HE staining.Flow cytometry analysis was applied to determine the apoptosis rate of SMMC-7721 cells.Results:(1) FN promoted the adhesion of human hepatoma cell strain SMMC-7721 in a dose-dependent manner.(2) rAdinbitor could dose-dependently inhibit the adhesion of SMMC-7721 cells to FN.The higher the concentration was,the stronger the inhibition was.There was significant difference among the groups (P＜0.05).(3) rAdinbitor had a strong inhibition on the proliferation of SMMC-7721 cells and showed a dose-dependent manner (P＜0.05).After a 48 h exposure,the IC5o value of rAdinbitor was 177.83 μg/mL.(4) After exposure of SMMC-7721 cells to 200 μg/mL rAdinbitor for 36 h,the eady morphologic changes appeared and the apoptosis rate was 20.68%,significantly higher than that of the control group (2.38%,P＜0.05).Conclusion:rAdinbitor can dose-dependently inhibit the SMMC-7721 cells adhesion to FN,and can inhibit the proliferation in dose-dependent manner and promote their apoptosis.     

姜黄素抗血管生成分子机制的探讨

目的:研究姜黄素抑制血管生成的分子机制。方法:采用MTT法、流式细胞术(FCM)观察姜黄素对人脐静脉内皮细胞(HUVECs)的抑制作用及促凋亡作用。采用RT-PCR法及Western-blot法检测姜黄素作用人肺腺癌A2细胞不同时间后血管生成素(Ang-1、Ang-2)、血小板反应素(TSP)mRNA的表达水平和血管内皮生长因子(VEGF),基质金属蛋白酶(MMP-9)的蛋白表达水平。结果:姜黄素能抑制HUVECs的增殖,呈时间及浓度依赖性,且能诱导HUVECs凋亡,凋亡率明显高于对照组(P<0.01)。A2细胞经100μmol/L姜黄素作用不同时间后Ang-1、Ang-2、TSPmRNA的表达率明显下降;VEGF与MMP-9的蛋白表达也明显减少。结论:姜黄素可能通过下列途径抑制肿瘤的血管生成:1)直接抑制血管内皮细胞增殖并促进其凋亡;2)抑制血管生成促进因子(VEGF,Ang-1,Ang-2)的表达;3)促进血管生成抑制因子TSP的表达;4)降低基质金属蛋白酶MMP-9的活性从而抑制细胞外基质降解。     

EFFECTS OF CURCUMIN ON PROLIFERATION AND APOPTOSIS OF HUMAN CERVICAL CARCINOMA HeLa CELLS IN VITRO

Curcumin,adeferuloymethane,isamajoractivecomponentofthefoodflavorturmetric(CurcumalLonga).Becauseofitsstablecolourandlusterandlowtoxicity,curcuminhasbeenwidelyusedasfoodadditiveandstain.Recently,ithasbeenreportedtopossesantiinflammatory,antioxidationandantiviralactivities.Now,attentionhasbeenfocusedonitsantitumoractivity[1].InvitrocurcuminwasfoundtoinduceapoptosisofawidevarietyoftumorcellsincludingmicesarcomaS180cells,humancoloncarcinomaHT-29cells,humanrenalcarcinoma293cells,humanlivercarcin…     

Effects of curcumin on bladder cancer cells and development of urothelial tumors in a rat bladder carcinogenesis model

Curcumin, a well-known dietary pigment derived from Curcuma longa, inhibited growth of several types of malignant cells both in vivo and in vitro. Its effects on cell proliferation and the induction of apoptosis in human bladder cancer cell lines and intravesical activity in a rat bladder tumor model were studied. Exposure of human bladder cancer cells to curcumin resulted in the induction of apoptotic cell death and caused cells to arrest in the G2/M phase. The anti-apoptotic Bcl-2 and Survivin protein was downregulated by the curcumin treatment together with enhancement of the Bax and p53 expression. The inhibitory activities of curcumin were stronger than those of cisplatin and could not be prevented by catalase pretreatment in T24 cells. Clonal assay indicated large-dose and short-term curcumin was lethal to bladder cancer cells. Moreover, the in vivo study revealed curcumin did induce apoptosis in situ, inhibit and slow the development of bladder cancer. These observations suggest that curcumin could prove an effective chemopreventive and chemotherapy agent for bladder cancer.     

Icariin,a natural flavonol glycoside,induces apoptosis in human hepatoma SMMC-7721 cells via a ROS/JNK-dependent mitochondrial pathway

In this study, the anticancer effect of icariin, a natural flavonol glycoside, against human hepatoma SMMC-7721 cells and the underlying mechanisms were investigated. Icariin triggered the mitochondrial/caspase apoptotic pathway indicated by enhanced Bax-to-Bcl-2 ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase cascade. Moreover, icariin induced a sustained activation of the phosphorylation of c-Jun N-terminal kinase (JNK) but not p38 and ERK1/2, and SP600125 (an inhibitor of JNK) almost reversed icariin-induced apoptosis in SMMC-7721 cells. In addition, icariin provoked the generation of reactive oxygen species (ROS) in SMMC-7721 cells, while the antioxidant N-acetyl cysteine almost completely blocked icariin-induced JNK activation and apoptosis. Taken together, these findings suggest that icariin induces apoptosis through a ROS/JNK-dependent mitochondrial pathway.     

奥沙利铂和人参皂苷Rg3不同联合方式对人肝癌细胞株SMMC-7721作用的影响

目的 通过体外实验观察奥沙利铂和人参皂苷Rg3不同联合方式对人肝癌细胞株SMMC-7721作用的影响,并初步探讨其机制。方法 采用MTT法观察奥沙利铂、人参皂苷Rg3单药以及两药同时和序贯应用对SMMC-7721细胞增殖的作用;应用流式细胞术分析单药和两药不同序贯方式对细胞周期分布及凋亡的影响;Western blotting检测单药和两药不同序贯方式作用后SMMC-7721细胞cyclin D1蛋白的表达情况。结果 奥沙利铂、人参皂苷Rg3单药、两药同时及序贯给药对SMMC-7721细胞增殖均有明显的抑制作用。同时用药组的增殖抑制作用优于人参皂苷Rg3先用组（P＜0.05）,但与奥沙利铂先用组比较未见明显差异（P＞0.05）;奥沙利铂先用组的效果优于人参皂苷Rg3先用组（P＜0.05）。流式细胞术分析显示,奥沙利铂主要将细胞阻滞在S期、G₂／M期,人参皂苷Rg3主要将细胞阻滞在G₀／G₁期,同时用药组和奥沙利铂先用组的凋亡率相似（P＞0.05）,阻滞细胞于G₂／M期,且凋亡率均较先用人参皂苷Rg3组高（P＜0.05）。Western blotting显示,两药序贯及同时应用组cyclin D1蛋白表达明显低于单药组,奥沙利铂先用组与同时用药组相似,均低于人参皂苷Rg3先用组。结论 奥沙利铂、人参皂苷Rg3序贯及同时应用较单药更能抑制人肝癌SMMC-7721细胞的增殖,先用奥沙利铂后序贯人参皂苷Rg3与两药同时应用的协同增效作用相似,均优于先用人参皂苷Rg3后序贯奥沙利铂,其机制可能与奥沙利铂先用组和同时用药组将细胞阻滞在S期、G₂／M期,增加促凋亡作用,同时下调cyclin D1蛋白的表达水平有关。