Activity Determination of 8 Chinese Herbs against Hepatoma Cell SMMC-7721 in Vitro by MTT Method

[Objective] The aim was to build up a set of efficient and rapid models for laboratory to screen anti-hepatocellular carcinoma active substance in vitro. [ Method] By using MTT method, the activities of anti-hepatocellular carcinoma SMMC-7721 in vitro from Cymbopogon distans, Lobelia chinensis, Buddleja offlcinalis, Glycyrrhiza uralensis, Sanguisorba officinalis, Bupleurum chinense, Apium graveolen and Curuma zedoaria were tested. The growth curve of hepatoma cell was described, and the growth status in different periods were observed by inverted microscope. [ Result] Cells induced by active substance would be condensing, clear brim, which have significant differences from normal SMMC- 7721 cells. The results suggested that ESCG, ESCC, ESCB could inhibit proliferation of SMMC-7721 cells at the concentration of 1.0 -1.5 mg/ml, and the inhibition rate were 51.6%, 48.5%, 52.9% respectively. With the increasing of concentration, the inhibition strengthened. [ Conclusion] MTT method could be used as a basic model for screening important anti-hepatoma.

Effects of cytotoxic T lymphocytes on hepatoma cell line SMMC-7721 induced by different subsets of dendritic cells in vitro

BACKGROUND: Dendritic cells (DCs) loaded with complex antigen are always used to induce cytotoxic T lymphocytes (CTLs) which have a specific anti-tumor activity. However, CTLs can assault autologous cells induced by DCs loaded with autologous antigen. This study aimed to explore how to weaken the autoimmune reaction induced by DC vaccine by combining mature DC (mDC) activating immunity and immature DC (imDC) leading to immune tolerance to make hepatocellular carcinoma (HCC) vaccine in vitro. METHODS: DC progenitors derived from human peripheral blood were assigned to two groups. One was cultured to mDC and pulsed with frozen-thawed antigen (FTA) of human HCC cell line SMMC-7721 cells (mDC group), and the other was cultured to imDC and pulsed with FTA of human liver cell line L-02 cells (imDC group). The morphology of DCs was monitored and cells phenotypes including HLA-DR, CD80, CD1α, CD83 were assayed by flowcytometry (FCM). The concentrations of interleukin-12 (IL-12) in the supernatant were assayed by ELISA. Methyl thiazolyl tetrazolium (MTT) was used to evaluate T cell proliferation induced by mDC and imDC and the killing rate of CTL induced by mDC and imDC respectively/together on SMMC-7721 and L-02 cells. RESULTS: Compared with the imDC group, the mDC group was characterized by the following: increased secretion of IL-12 (P【0.05); higher expression of HLA-DR, CDla, CD80, CD83; and stronger activity in stimulating proliferation of isogenic T cells (P【0.05). CTL induced by the mDC group had a significant killing response to SMMC-7721 as well as a higher killing rate for L-02 (P】0.05). CTL induced by mDC and imDC together had a higher killing response to SMMC-7721, but a lower killing rate for L-02(P【0.01). CONCLUSIONS: CTL induced by mDC and imDC together has a higher antigen-specific killing response in vitro than that induced by mDC alone. This may be of greater clinical value.

Downregulation of alpha-fetoprotein siRNA inhibits proliferation of SMMC-7721 cells

AIM: To study the function of α-fetoprotein (AFP) in SMMC-7721 hepatoma cells.METHODS: A hairpin siRNA expressing plasmid pSilencer3.0-H1-afp was constructed and transfected into SMMC-7721 cells with Lipofectamine 2000. The expression of AFP was monitored by real-time RT-PCR and immunoassays, its effect on SMMC-7721 cell proliferation and cell death was detected by MTT and fluorescenceactivated cell sorter (FACS).RESULTS: The AFP-siRNA expressing plasmid downregulated the expression of AFP obviously (about 34%), and inhibited SMMC-7721 cell proliferation, but did not induce apoptosis.CONCLUSION: Downregulation of AFP siRNA inhibits proliferation of SMMC-7721 cells, but cannot cause apoptosis.

Protein profile of human hepatocarcinoma cell line SMMC-7721:Identification and functional analysis

AIM： TO investigate the protein profile of human hepatocarcinoma cell line SMMC-7721, to analyze the specific functions of abundant expressed proteins in the processes of hepatocarcinoma genesis, growth and metastasis, to identify the hepatocarcinoma-specific biomarkers for the early prediction in diagnosis, and to explore the new drug targets for liver cancer therapy. METHODS： Total proteins from human hepatocarcinoma cell line SMMC-7721 were separated by two-dimensional electrophoresis （2DE）. The silver-stained gel was analyzed by 2DE software Image Master 2D Elite. Interesting protein spots were identified by peptide mass fingerprinting based on matrix-assisted laser desorption/ ionization time-of-flight mass spectrometry （MALDI-TOF-MS） and database searching. RESULTS： We obtained protein profile of human hepatocarcinoma cell line SMMC-7721. Among the twenty-one successfully identified proteins, mitofilin, endoplasmic reticulum protein ERp29, ubiquinol-cytochrome C reductase complex core protein I, peroxisomal enoyl CoA hydratase, peroxiredoxin-4 and probable 3-oxoacid CoA transferase 1 precursor were the six novel proteins identified in human hepatocarcinoma cells or tissues. Specific functions of the identified heat-shock proteins were analyzed in detail, and the results suggested that these proteins might promote tumorigenesis via inhibiting cell death induced by several cancer-related stresses or via inhibiting apoptosis at multiple points in the apoptotic signal pathway. Other identified chaperones and cancer-related proteins were also analyzed.CONCLUSION： Based on the protein profile of SMMC-7721 cells, functional analysis suggests that the identified chaperones and cancer-related proteins have their own pathways to contribute to the tumorigenesis, tumor growth and metastasis of liver cancer. Furthermore, proteomic analysis is indicated to be feasible in the cancer study.

Positional and expressive alteration of prohibitin during the induced differentiation of human hepatocarcinoma SMMC-7721 cells

AIM： To explore the existence and distribution of prohibitin （PHB） in nuclear matrix and its co-localization with products of some related genes during the differentiation of human hepatocarcinoma SNMC-7721 cells. METHODS： The nuclear matrix of the SMMC-7721 cells cultured with or without 5 × 10^-3 mmol/L hexamethylene bisacetamide （HNBA） was selectively extracted. Western blot was used to analyze the expression of PHB in nuclear matrix; immunofluorescence microscope observation was used to analyze the distribution of PHB in cell. LCSM was used to observe the co-localization of PHB with products of oncogenes and tumor suppressor genes. RESULTS： Western blot analysis showed that PHB existed in the composition of nuclear matrix proteins and was down-regulated by HMBA treatment. Immunofluorescence observation revealed that PHB existed in the nuclear matrix, and its distribution regions and expression levels were altered after HMBA treatment. Laser scanning confocal microscopy revealed the co-localization between PHB and the products of oncogenes or tumor repression genes including c-los, c-myc, p53 and Rb and its alteration of distributive area in the cells treated by HMBA. CONCLUSION： These data confirm that PHB is a nuclear matrix protein, which is located in the nuclear matrix, and the distribution and expression of PHB and its relation with associated genes may play significant roles during the differentiation of SMMC-7721 cells.

Combined anti-tumor effects of mDRA-6 and nimesulide on human hepatocellular cancer cell line SMMC-7721

Objective: The aim of this work was to evaluate anti-tumor effects of mDRA-6 plus nimesulide on a human hepatocellular cancer cell line, SMMC-7721, and study the main mechanisms. Methods: The DR5 receptor of SMMC-7721 cells was detected by flow cytometry (FCM). For further experimental application, SMMC-7721 cells were treated with proper dose of mDRA-6, nimesulide, or mDRA-6 plus 200 μmol/L nimesulide; untreated SMMC-7721 cells were comparably set as control. Cytotoxicity was tested by MTT assay; cell morphology was examined using Hoechst 33258 staining; and apoptosis was determined by FCM. Results: The positive rate of DR5 on SMMC-7721 was 95.0%. Either mDRA-6 or nimesulide alone induces SMMC-7721 cell death in a dose-dependent manner. Treatment of 1,600 ng/mL mDRA-6 for 12h led to a cell-death rate of 35.0%, while an increased cell-death rate (91.1%) was found under the same condition of mDRA-6 treatment supple- mented with 200 μmol/L nimesulide. Hoechst 33258 and Annexin V/PI staining confirmed apoptosis as the main cause of this anti-tumor response. Conclusion: Both mDRA-6 and nimesulide can induce apoptosis of SMMC-7721 cells, and they have synergistic anti-tumor activities against SMMC-7721.

Modulating effects of survivin antisense oligonucleotide on changes of apoptosis and cell cycle of human hepatocellular carcinoma cell line SMMC-7721

To investigate the modulating effects of survivn antisense oligonucletode (ASODN) on the cell cycle and apoptosis of human hepatocellular carcinoma (HCC) cell line SMMC-7721 and explore its mechanism.Methods Survivin ASODN was transfected into SMMC-7721 cells mediated by DOTAP liposomal reagent.Electron microscopy,flow cytometry and RT-PCR were used to detect the changes in cell ultrastructure,apoptosis,cell cycle and the expression of cyclinB1 mRNA,respectively.Results After transfection of survivin ASODN,the expression of cyclinB1 mRNA in the cells significantly increased and increase in G2-M arrest and apoptosis appeared.Meanwhile,the cell ultrastructure had apoptotic changes such as chromatin condensation and apoptotic body formation.Conclusion Survivin ASODN can induce the expression of cyclinB1 that may result in G2-M arrest.Consequently,apoptosis is triggered.Survivin ASODN transfection might be an improtant new treatment for HCC.14 refs,2 figs,1 tab.

刺梨三萜对人肝癌SMMC-7721细胞增殖的影响

目的:观察刺梨三萜(Rosa roxburghii Tratt triterpene,RRTT)对人肝癌细胞SMMC-7721细胞增殖的影响,研究其可能的作用机制。方法:采用形态学观察和MTT法分析RRTT对SMMC-7721细胞增殖的影响;通过NBT还原实验和细胞培养上清液中甲胎蛋白(alpha-fetoprotein,AFP)含量的测定分析RRTT对SMMC-7721分化的影响;采用AO/EB染色法和FCM检测RRTT对肿瘤细胞周期和细胞凋亡的影响;RT-PCR检测Bad mRNA的表达。结果:RRTT对SMMC-7721细胞增殖的抑制作用呈时间和剂量依赖性。与阴性对照组比,随RRTT剂量的增加,NBT阳性细胞比率增加,AFP含量逐渐降低。RRTT对SMMC-7721细胞凋亡和增殖周期均无明显影响。RRTT作用后,Bad mRNA的表达下调。结论:RRTT具有体外抗SMMC-7721作用,其机制可能通过下调Bad mRNA的表达而诱导细胞分化,而与抑制细胞增殖和诱导细胞凋亡无关。

壳寡糖抑制肝癌细胞SMMC-7721的增殖及其机制探讨

探讨壳寡糖抑制人肝癌细胞株SMMC-7721的增殖作用及其分子机制。采用噻唑蓝(MTT)法检测壳寡糖的细胞增殖抑制作用;利用流式细胞仪检测肝癌细胞的凋亡情况;用RT-PCR和Western blot方法研究壳寡糖引起凋亡的原因。结果显示,0.8mg/mL的壳寡糖能够抑制SMMC-7721细胞增殖,并且促进SMMC-7721细胞的凋亡,其原因是壳寡糖能够上调促凋亡蛋白Bax的表达。

斑蝥素酸镁阻断MAPK信号通路抑制SMMC-7721人肝癌细胞增殖

目的观察斑蝥素酸镁对SMMC-7721肝癌细胞丝裂原激活蛋白激酶(MAPK)信号通路的影响,探讨斑蝥素酸镁的抗癌机制。方法使用蛋白磷酸酶2A(PP2A)活性检测试剂盒分别检测斑蝥素酸镁和冈田酸(OA)对PP2A活性的影响。实时定量PCR检测斑蝥素酸镁、OA对SMMC-7721人肝癌细胞胞外信号调节激酶1/2(ERK1/2)、p38MAPK、c-Jun N末端激酶1/2(JNK1/2)mRNA表达水平的影响;Western blot法检测斑蝥素酸镁、OA对SMMC-7721细胞ERK1/2、p38MAPK、JNK蛋白表达以及蛋白磷酸化水平的影响。结果 0.283μmol/L斑蝥素酸镁对PP2A活性无明显抑制作用,0.567μmol/L斑蝥素酸镁能显著抑制PP2A活性,且随着药物浓度的增加,抑制作用愈趋明显;同时0.059 nmol/L OA对PP2A活性也有显著抑制作用。与空白对照组比较,0.283μmol/L斑蝥素酸镁组ERK1、ERK2 mRNA表达量无明显变化,当浓度为0.567μmol/L时,ERK1、ERK2mRNA表达量显著下降,且随着药物浓度的增加下降更明显;而0.059 nmol/L OA组ERK1、ERK2 mRNA表达量却显著升高。0.059 nmol/L OA和不同浓度斑蝥素酸镁组的p38MAPK、JNK1、JNK2 mRNA表达量均显著升高。与空白对照组比较,0.283μmol/L斑蝥素酸镁组ERK1/2磷酸化水平无明显变化,高于0.567μmol/L斑蝥素酸镁处理显著下调ERK1/2磷酸化水平,其下调程度具有浓度依赖效应;而0.059 nmol/L OA组ERK1/2磷酸化水平却显著上调。0.059 nmol/L OA和不同浓度斑蝥素酸镁组的p38MAPK、JNK磷酸化水平均显著上调。结论斑蝥素酸镁可能是通过抑制PP2A活性进而抑制ERK1/2通路来实现对SMMC-7721肝癌细胞增殖的抑制作用。

白毛藤提取物对肝癌SMMC-7721细胞增殖及c-myc基因表达的抑制作用

目的观察白毛藤水提液对人肝癌SMMC-7721细胞增殖及c-myc基因mRNA表达水平的影响,探讨中药白毛藤的抗癌作用机制。方法用不同浓度白毛藤水提取物处理肝癌SMMC-7721细胞,观察细胞形态变化,用台盼兰染色并作细胞计数,cck-8试剂盒检测不同药物浓度组的细胞增殖抑制情况。RT-PCR检测c-myc基因mRNA表达水平。结果倒置显微镜下可见给药组细胞数目明显减少,且随药物浓度增加其抑制效果增强。WST-8法显示,在药物浓度为2,4,8,16 mg/ml时,细胞增殖明显受到剂量依赖性抑制,其抑制率分别为24.37%,50.07%,66.14%,83.23%。细胞中c-myc基因mRNA表达水平降低,并与药物浓度呈明显的量效关系。结论白毛藤可显著抑制人肝癌SMMC-7721细胞的增殖,下调c-myc基因mRNA表达,这可能是白毛藤的抗癌作用的部分机制。

水红花子黄酮类成分对人肝癌细胞株SMMC-7721的影响

目的:研究水红花子黄酮类成分对人肝癌细胞株SMMC-7721增殖、细胞周期及细胞凋亡的影响。方法:采用MTT法研究水红花子黄酮类成分对人肝癌细胞SMMC-7721的抑制作用及时效量效关系;并通过PI染色法和Annexin V-EGFP/PI双染法观察水红花子黄酮类成分作用于人肝癌细胞株SMMC-7721后细胞周期DNA含量变化及细胞凋亡率。结果:水红花子黄酮类成分能调节SMMC-7721人肝癌细胞株G1/S转换,使肿瘤细胞发生S期阻滞,造成S期细胞堆积,阻断细胞的DNA合成和复制,阻滞肿瘤细胞进入G2/M期,从而抑制肿瘤细胞的增殖,诱导SMMC-7721细胞凋亡,且具有明显的时效及量效关系。结论:水红花子黄酮类成分对人肝癌细胞株SMMC-7721具有明显的抑制作用,且抑制作用和时间剂量成线性关系,其作用机制为抑制肿瘤细胞的增殖和诱导该细胞的凋亡。

白花丹醌对人肝癌细胞HepG2、SMMC-7721增殖及其Bax/Bcl-2、Cyclin D1 mRNA表达的影响

目的探索白花丹醌对人肝癌细胞HepG2、SMMC-7721增殖的影响及其影响机制。方法人肝癌细胞HepG2和SMMC-7721分别与白花丹醌共培养,通过显微图像、MTT法检测了白花丹醌对上述两种肝癌细胞增殖情况的影响,利用实时荧光定量PCR(Qpcr)检测其Bax/Bcl-2,Cyclin D1mRNA表达的影响。结果显微照像和MTT法测定都表明白花丹醌能明显地抑制两种肝癌细胞的增殖;Qpcr检测表明,对HepG2和SMMC-7721,白花丹醌能明显上调Bax/Bcl-2mRNA比值(P=0.0017和P=0.00104),同时明显下调Cy-clin D1 mRNA水平(P=0.0287和P=0.0165)。结论白花丹醌能抑制HepG2、SMMC-7721的增殖,其机制与Bax/Bcl-2比值上升和Cyclin D1转录水平下降有关。

白茅根水提物对人肝癌细胞株SMMC-7721细胞周期及细胞凋亡的影响

目的研究白茅根水提物对人肝癌细胞株SMMC-7721增殖抑制率、细胞周期及细胞凋亡的影响。方法采用MTT法研究白茅根水提物对人肝癌细胞SMMC-7721的抑制率及抑制率与时间剂量关系;并通过PI染色法和Annexin V-EGFP/PI双染法研究白茅根水提物作用于人肝癌细胞株SMMC-7721后细胞周期DNA含量变化及对细胞凋亡率的影响。结果不同浓度的白茅根水提物处理肝癌SMMC-7721细胞24,48,72,96 h后,均呈现出显著的细胞增殖抑制作用,抑制作用具有明显的时间-剂量-效应关系,差异有统计学意义(P<0.05);细胞周期与细胞凋亡实验结果显示不同浓度的白茅根水提物处理肝癌SMMC-7721细胞46 h后可显著增加肝癌细胞凋亡率,差异有统计学意义(P<0.001),作用36 h后,可增加S期比例同时降低G2/M期细胞比例,差异有统计学意义(P<0.001)。结论白茅根水提物对人肝癌细胞株SMMC-7721具有明显的增殖抑制作用并可诱导其凋亡,该作用是通过抑制G2/M期细胞比例,将细胞周期阻滞在S期实现的。

热疗对SMMC-7721肝癌细胞形态、增殖、凋亡的影响

目的探讨热疗对SMMC-7721肝癌细胞的影响。方法将SMMC-7721肝癌细胞置恒温循环水浴锅中(42.5±0.5)℃孵育1h,然后放入37℃、5%CO2的培养箱中继续培养,分别于热处理后0、6、12、24h采用倒置显微镜(LM×400)观察细胞形态变化,采用四甲基偶氮唑蓝(MTT)法检测细胞增殖,予Annexin V/PI染色后用流式细胞仪检测细胞凋亡,予366EC和FITC-羊抗鼠IgG处理细胞后用流式细胞仪检测细胞DR5表达,用Fluo-3/AM负载细胞检测胞内Ca2+浓度的变化。结果热疗可导致肿瘤细胞形态改变,表现为细胞变小,变圆,脱落,出现空泡;热疗可抑制细胞增殖,细胞热疗后0、6、12、24h细胞抑制率分别为22.18%、26.76%、31.30%、36.62%。热疗后0h细胞凋亡率为15.00%,其中早期凋亡率为2.00%,晚期凋亡率为13.00%;热疗后6h细胞凋亡率为65.45%,其中早期凋亡率为43.23%,晚期凋亡率为22.22%;热疗后12h细胞凋亡率为12.32%,其中早期凋亡率为4.60%,晚期凋亡率为7.72%;热疗后24h细胞凋亡率为22.58%,其中早期凋亡率为7.15%,晚期凋亡率为15.43%。热疗后0、4、8、12、24h细胞内钙离子浓度分别为18.13、7.87、13.01、37.23μmol/L,对照组为14.28μmol/L。热疗后0、6、12、24h细胞膜DR5表达率分别为79.74%、83.22%、91.28%、92.52%,对照组为83.02%。结论热疗导致肿瘤细胞凋亡的因素是复杂的,DR5表达增加和细胞内Ca2+增加是原因之一;热疗可增加肿瘤细胞DR5的表达,提示热疗加化疗或其他治疗可能会增加疗效。

MTT法测定8种中草药体外抗肝癌细胞SMMC-7721活性

[目的]建立一套适合于实验室高效、快速的体外抗肝癌活性物质筛选模型。[方法]通过MTT法,对芸香草、半边莲、蜜蒙花、甘草、地榆、柴胡、旱芹和莪术等8种中草药体外抗肝癌细胞SMMC-7721的活性进行初测;描绘肿瘤细胞生长曲线,倒置显微镜观察细胞不同阶段的生长状况。[结果]受活性物质作用细胞尽管仍然贴壁,但萎缩,边缘清晰化,与生长状况良好的细胞形态有明显区别;浓度为1.0～1.5mg/ml的甘草乙醇浸提液(ESCG)、莪术乙醇浸提液(ESCC)和柴胡乙醇浸提液(ESCB)对体外培养的肝癌细胞SMMC-7721有较强的抑制增殖作用,抑制率分别为51.6%、48.5%和52.9%,且抑制作用随着浓度的增加而加强。[结论]MTT法筛选可作为重要抗肿瘤的1个基本筛选模型。

黄芩苷对肝癌细胞株SMMC-7721裸鼠移植瘤生长抑制作用及其机制

目的:以裸鼠人肝癌细胞株SMMC-7721移植瘤动物模型为研究对象,观察黄芩苷对移植瘤生长能力的影响,初步探讨黄芩苷对Cyclin D1和Caspase-3表达的影响。方法:BALB/c裸鼠右前腋部皮下接种人肝癌SMMC-7721细胞5×106个,建立人肝癌实体瘤模型。将20只成瘤裸小鼠随机分为空白对照组与黄芩苷组,每组10只。对照组腹腔注射生理盐水10ml/kg,黄芩苷组腹腔注射黄芩苷注射液100mg/kg,每2d给药1次,间断给药8次后称体重、处死,瘤块离体称重,计算抑瘤率;用免疫组织化学方法检测实验组和对照组移植瘤中CyclinD1和Caspase-3的表达水平。结果:黄芩苷组100mg/kg对裸鼠肝癌SMMC-7721实体瘤的抑制率为30.8%,两组间肝脏与肾脏指数比较,P均大于0.05。黄芩苷处理组凋亡指数为(13.6±1.1)%,高于对照组的(2.2±1.9)%,(P<0.01)。黄芩苷能够抑制CyclinD1表达及上调Caspase-3表达,(均P<0.05)。结论:黄芩苷对人肝癌SMMC-7721的裸鼠皮下移植瘤具有生长抑制作用,其抑瘤作用可能通过下调CyclinD1表达和上调Caspase-3表达来达到抑制瘤体增殖并有促进其凋亡的作用。在保护免疫器官功能方面,黄芩苷无明显优势。黄芩苷可能成为治疗原发性肝癌的有效手段之一,但是其在保护免疫器官方面还需要进一步研究。

消癌平与奥沙利铂及恩度联合对人肝癌细胞株SMMC-7721的体外增殖抑制实验

目的:通过体外实验研究消癌平(Xiaoaiping,XAP)注射液、奥沙利铂(oxaliplatin,L-OHP)、恩度(Endostar,重组人血管内皮抑制素)单药及其与XAP的两药及三药联合应用对人肝癌SMMC-7721增殖的影响,探讨其联合用药的理论依据.方法:采用MTT法观察XAP、L-OHP、恩度单药及其XAP的两药及三药联合应用对人肝癌SMMC-7721细胞增殖抑制作用,并观察细胞形态的变化.结果:10-40μL/mL XAP和1-4μg/mL L-OHP对SMMC-7721均有明显的抑制作用,并呈时间和浓度依赖性(P<0.01和P<0.05).1-12μg/mL恩度对该细胞无增殖抑制作用.20μL/mL XAP和1μg/mL L-OHP联合对SMMC-7721细胞增殖抑制率分别为82.08%,优于对照组(P<0.01),联合具有相加作用.20μL/mL XAP与6μg/mL恩度联合则具有明显的协同作用.三药联合抑制作用更明显.结论:XAP、L-OHP单药能抑制肝癌细胞增殖;恩度无抑制作用;与XAP两药联合对肝癌细胞增殖有协同增效作用,三药联合作用更明显.

消癌解毒方含药血清诱导人肝癌SMMC-7721细胞凋亡的实验研究

目的探讨消癌解毒方的抗肿瘤作用机理。方法消癌解毒方含药血清作用人肝癌SMMC-7721细胞后,采用电镜技术观察细胞的形态改变,流式细胞仪Annexin V-FITC法检测细胞凋亡情况。结果消癌解毒方能明显促进肝癌细胞的凋亡。电镜下SMMC-7721细胞出现明显的细胞凋亡的形态学改变;凋亡作用以高剂量组效果最佳,凋亡率与顺铂组相似(P>0.05)。结论消癌解毒方通过诱导人肝癌SMMC-7721细胞凋亡抑制其生长。

3-溴丙酮酸对SMMC-7721肝癌细胞增殖的抑制作用

目的观察3-溴丙酮酸(3-BrPA)对SMMC-7721肝癌细胞增殖的抑制作用。方法对经0.25mmol/L～8.00mmol/L3-BrPA溶液处理的SMMC-7721细胞,采用MTT法检测细胞增殖抑制情况,并在荧光显微镜和电镜下观察细胞内部结构的变化。结果3-BrPA对SMMC-7721细胞的增殖有明显的抑制作用,其中在0.75mmol/L浓度下的抑制作用最强;经处理后的细胞,在荧光染色下显示坏死细胞增多,在电镜下显示细胞染色质分散,少量核染色质凝聚。结论3-BrPA对SMMC-7721肝癌细胞有抑制作用。