人参皂甙对肺癌细胞和血管内皮细胞增生、凋亡及其周期的影响

目的：探讨中药20(R)-人参皂甙Rg3(Rg3)对肺癌细胞和血管内皮细胞增生、凋亡以及细胞周期的影响。方法：进行人肺腺癌细胞株A549、人脐静脉血管内皮HUVEC304细胞培养,不同浓度Rg3干预,采用MTT法、流式细胞术、透射电镜等技术,了解不同浓度Rg3对上述细胞增生、凋亡以及细胞周期的影响。结果：3×10-6 mol/L的Rg3可导致A549细胞明显凋亡,凋亡率为29.8%,与对照组(15.0%)相比差异有统计学意义（P<0.05）。Rg3对A549细胞周期的影响无显著差异。1×10-4 mol/L的Rg3对内皮细胞的生长抑制率为12.53%,显著高于其它组（P<0.05）,不同浓度Rg3对条件培养液（CM）诱导的血管内皮细胞的增生均有明显的抑制作用（P<0.05）,电镜下可见10-6 mol/L浓度的Rg3可使CM诱导的内皮细胞出现凋亡小体。 结论：适当浓度的Rg3有抗肿瘤作用和抑制肿瘤新生血管生成的作用。     

人参皂苷Rg1 对阿霉素引起的血管内皮细胞 损伤的作用及机制研究

目的 探讨人参皂苷Rg1 对阿霉素损伤后血管内皮细胞的作用及其机制。方法 该研究分为 正常组、阿霉素组（0.5μg/ml）、阿霉素+Rg1 组（0.5μg/ml 阿霉素+200μg/ml Rg1）。通过MTT 法、划 痕及小管形成实验检测人参皂苷Rg1 对阿霉素损伤后血管内皮细胞增殖、迁移及小管形成的影响。通过 Hochst33342 染色和流式细胞术检测人参皂苷Rg1 对阿霉素损伤后血管内皮细胞凋亡的影响。采用Western blotting 检测人参皂苷Rg1 对阿霉素损伤后血管内皮细胞Bcl-2、p-Akt、p-ERK 及p-eNOS 蛋白表达的影 响。结果 与正常组比较,阿霉素组细胞活性降低（P <0.05）;与阿霉素组比较,阿霉素+Rg1 组能提高血管 内皮细胞的细胞活性（P <0.05）。与阿霉素组比较,阿霉素+Rg1 组能够改善血管内皮细胞的迁移及小管形 成状态（P <0.05）。与阿霉素组比较,阿霉素+Rg1 组减少阿霉素引起的细胞凋亡（P <0.05）。与阿霉素组比较, 阿霉素+Rg1 组阿霉素损伤后血管内皮细胞NO 升高（P <0.05）,ROS 减少（P <0.05）。阿霉素组Bcl-2、 p-ERK、p-Akt 及p-eNOS 蛋白相对表达量较正常组低（P <0.05）,阿霉素+Rg1 组较阿霉素组高（P <0.05）。 结论 人参皂苷Rg1 可减轻阿霉素引起的血管内皮细胞损伤,从而为人参皂苷Rg1 治疗阿霉素引起的心脏损 伤提供新的靶点。     

人参皂苷 Rg3对人鼻咽癌 CNE -2细胞血管生成拟态及迁移能力的影响

目的：探讨人参皂苷 Rg3对人低分化鼻咽癌细胞系 CNE -2体外血管生成拟态及迁移能力的影响。方法用不同浓度（0、38、76和114μmol/ L）的 Rg3处理 CNE -2细胞后,体外管道形成抑制实验检测 Rg3对CNE -2细胞管道形成能力的影响;Transwell 小室法检测 Rg3对 CNE -2细胞迁移能力的影响;Western blot 法检测 Rg3对 CNE -2细胞中 COX -2、HIF -1α、VEGF 和 Fascin1蛋白表达的影响。结果人参皂苷 Rg3能抑制 CNE -2细胞体外管道形成的能力,其管状结构数量与 Rg3浓度呈负相关（P ＜0.01）;Rg3浓度大于76μmol/ L 时可以抑制 CNE -2细胞的迁移能力,与0μmol/ L Rg3比较差异有统计学意义（P ＜0.05）;且 Rg3对 COX -2、HIF -1α、VEGF 和 Fascin1蛋白表达的影响趋势分别与 Rg3对血管生成拟态和迁移能力的变化趋势呈正相关（ P ＜0.05）。结论人参皂苷 Rg3能抑制 CNE -2细胞体外血管生成拟态及迁移能力,其分子机制可能与抑制 CNE -2细胞中COX -2、HIF -1α、VEGF 和 Fascin1蛋白的表达有关。     

人参皂苷Rg3通过调控PXN-AS1促进肺癌放射增敏的机制探讨

目的 探讨人参皂苷Rg3调控长链非编码RNA(long noncoding RNA,LncRNA)PXNAS1的表达及对肺癌细胞放射敏感性的影响。方法 选用肺癌细胞株A549、H466、H1299、H522,将培养液中加入人参皂苷Rg3的肺癌细胞确定为研究组,未加药物培养的肺癌细胞为对照组。进行克隆形成实验,检测人参皂苷Rg3对肺癌细胞放射敏感性的影响。流式细胞仪检测人参皂苷Rg3对肺癌细胞凋亡的作用。通过荧光定量PCR检测肺癌组织和细胞中PXN-AS1的表达。结果 与对照组比较,研究组人参皂苷Rg3能够明显降低肺癌细胞放射治疗后的克隆形成率(P<0.05),显著增加细胞凋亡(P<0.05)。PXN-AS1在肺癌组织和细胞中高表达,且与肺癌患者的预后呈负相关。加入人参皂苷Rg3后,研究组PXN-AS1的表达发生明显下调(P<0.05)。结论 人参皂苷Rg3可能是潜在的放射增敏剂,可能通过调控PXN-AS1促进肺癌的放射增敏。     

心肌成纤维细胞诱导体外血管新生的实验研究

目的探讨心肌成纤维细胞在血管新生中的作用。方法分离培养乳鼠心肌成纤维细胞(cardiac fibroblasts,CF),并收集其条件培养液(cardiacfibroblastconditionedmedium,CF CM)作为ECV304[人脐静脉内皮细胞株(humanumbilicalveinendothelialcellstrain)]细胞的培养液,用3H TdR掺入法检测CF CM对ECV304细胞增殖活性的影响;采用体外血管新生三维模型,检测其是否能诱导ECV304细胞向凝胶内侵入。结果乳鼠心肌成纤维细胞的条件培养液明显促进ECV304细胞增殖(P<0.01),诱导ECV304细胞向凝胶内侵入迁移生长,形成树枝样发芽结构。结论心肌成纤维细胞的条件培养液可促进ECV304细胞增殖和迁移,即有促血管新生作用。     

20（R）-人参皂苷Rg 3对人乳腺癌细胞自噬作用的影响

目的：观察20(R)-人参皂苷Rg3对人乳腺癌细胞（MCF-7）自噬作用的影响,并探讨20(R)-人参皂苷Rg3诱导MCF-7自噬作用的最佳剂量。方法人乳腺癌细胞株分为20(R)-人参皂苷Rg3实验组及空白对照组。采用MTT法观察20(R)-人参皂苷Rg3对MCF-7细胞生长的抑制作用,并依据计算出的IC50值确定20(R)-人参皂苷Rg3的有效浓度。结果当20(R)-人参皂苷Rg3浓度在37.5～600.0mg/L时,MCF-7细胞的生长抑制率最高,并随其浓度的增加而增大,与对照组比较差异有统计学意义（P＜0.05）。在荧光显微镜下观察到细胞所含自噬泡明显增多,说明20(R)-人参皂苷Rg 3可诱导乳腺癌细胞自噬。蛋白质印迹法检测结果显示：LC 3蛋白,特别是LC 3-I 的表达量与细胞自噬程度呈正相关,随着20(R)-人参皂苷Rg 3干预浓度的增大,LC3-I和LC3-I蛋白表达量亦明显升高,与对照组比较差异有统计学意义（P＜0.05）。结论20(R)-人参皂苷Rg3能显著抑制MCF-7细胞的增殖,且呈现良好的剂量、时间依赖性;20(R)-人参皂苷Rg 3有诱导MCF-7细胞自噬作用。     

20（R）-人参皂苷Rg_3抗血小板活化因子诱导血管内皮细胞损伤的保护作用

目的探讨20（R）-人参皂苷Rg3抗血小板活化因子（PAF）损伤人脐静脉血管内皮细胞（HUVEC）的保护作用及其机制.方法采用MTT法测定PAF诱导HUVEC活性;用双波长荧光分光光度法测定HUVEC细胞内游离钙离子浓度;用ELISA法测定培养的细胞上清液中t-PA、PAI-1含量.结果 1μmol/LPAF刺激HUVEC 2 h后,可明显降低HUVEC的吸光度值,细胞内钙离子浓度升高,上清液中PAI-1含量明显升高,而t-PA含量无明显变化;20～80μmo/L 20（R）-人参皂苷Rg3可升高HUVEC吸光度值,并呈浓度依赖性显著降低HUVEC内游离钙浓度;20（R）-人参皂苷Rg3降低上清液中PAI-1含量,对t-PA含量无明显影响.结论 20（R）-人参皂苷Rg3对PAF诱导损伤的HUVEC具有抗损伤保护作用,其机理可能与降低细胞内钙离子浓度,抑制PAI-1产生和调节t-PA/PAI-1平衡作用有关.     

5种不同中药组合对血管内皮细胞生物活性的影响

目的比较5种不同中药组合对人微血管内皮细胞株(HMEC-1)生物活性的影响,为抗肿瘤血管形成复方中药的研制提供依据。方法设置7个组,A组(阴性对照组)为生理盐水,B_1组为藤黄酸+人参皂苷Rg3+斑蝥素,B_2组为藤黄酸+人参皂苷Rg3+青蒿琥脂,B_3组为斑蝥素+人参皂苷Rg3+青蒿琥脂,B_4组为藤黄酸+人参皂苷Rg3,B_5组为藤黄酸+苦参碱,C组(阳性对照组)为沙利度胺。药物浓度:藤黄酸为20μg/mL,去甲斑蝥素为20μg/mL,人参皂苷Rg3为100μg/mL,青蒿琥脂为150μg/mL,苦参碱为100μg/mL,沙利度胺为50μg/mL。每孔加每种药物100μL,每组设6个复孔。比较每组HMEC-1细胞增殖、黏附、迁移、体外血管形成能力。结果 5种不同中药组合中,藤黄酸+人参皂苷Rg3+斑蝥素组合抑制血管内皮细胞增殖、黏附、迁移、体外血管形成效果最好,其次是藤黄酸+人参皂苷Rg3+青蒿琥脂组合,第3是人参皂苷Rg3+斑蝥素+青蒿琥脂组合,第4是藤黄酸+人参皂苷Rg3组合,第5是藤黄酸+苦参碱组合,与生理盐水组比较,差异有统计学意义(均P<0.05)。结论藤黄酸+人参皂苷Rg3+斑蝥素组合具有较强的抑制血管内皮细胞生物学活性的效果。     

人参皂苷Rg3对胃癌肝转移患者血清VEGF的影响

胃癌是常见的消化道恶性肿瘤之一,肝转移发 生率高,是影响预后的主要因素之一。肿瘤血管生 成是胃癌生长与转移的重要条件,需要多种因素调 节[1],而血管内皮细胞生长因子（VEGF）是目前已知 最强的直接作用于血管内皮细胞的生长因子,与肿 瘤的复发、转移及预后密切相关[2]。人参皂苷Rg3是 一种人参二醇类四环三萜皂苷,分子式 C42H72O13, 分子量 785.02,为我国自主开发的新型重组人血管 内皮抑素,具有多靶点抗肿瘤血管生成作用。本研 究以人参皂苷Rg3和（或）化疗治疗胃癌肝转移患者 56例,观察患者血清VEGF水平变化,现将结果报道 如下。     

人参皂苷Rg3抗血管形成作用的实验研究

目的:探讨人参皂苷Rg3的抗血管形成作用.方法:原代培养人脐静脉内皮细胞(HUVEC),四甲基偶氮唑盐(MTT)法检测TNP-470(阳性对照)和人参皂苷Rg3对HUVEC增生的影响;采用改良鸡胚绒毛尿囊膜新生血管形成模型,将不同剂量人参皂苷Rg3和TNP-470(阳性对照)置于7天的鸡胚绒毛尿囊膜上,3天后观察新生血管形成是否被抑制.结果:TNP-470抑制HUVEC增生,人参皂苷Rg3对HUVEC增生无影响,二者都抑制鸡胚绒毛尿囊膜新生血管形成.结论:人参皂苷Rg3无细胞毒作用,但有抗血管形成作用.     

Inhibitory effect of ginsenoside Rg3 on ovarian cancer metastasis

Background Ginsenosides are main components extracted from ginseng, and ginsenoside Rg3 is one of the most important parts. Ginsenoside Rg3 has been found to inhibit several kinds of tumor growth and metastasis. The present study was undertaken to investigate the effect of ginsenoside Rg3 on human ovarian cancer metastasis and the possible mechanism. Methods The experimental lung metastasis models of ovarian cancer SKOV-3 and the assay of tumor-induced angiogenesis were used to observe the inhibitory effects of Rg3 on tumor metastasis and angiogenesis. The effect of Rg3 on invasive ability of SKOV-3 cells in vitro was detected by Boyden chamber, and immunofluorescence staining was used to recognize the expression of matrix metalloproteinase 9 （MMP-9） in SKOV-3 cells. Results In the experimental lung metastasis models of ovarian cancer, the number of tumor colonies in the lung and vessels oriented toward the tumor mass in each ginsenoside Rg3 group, was lower than that of control group. The invasive ability and MMP-9 expression of SKOV-3 cells decreased significantly after treatment with ginsenoside Rg3. Conclusions Ginsenoside Rg3 can significantly inhibit the metastasis of ovarian cancer. The inhibitory effect is partially due to inhibition of tumor-induced an qioqenesis and decrease of invasive ability and MMP-9 expression of SKOV-3 cells.     

Inhibitory effect of ginsenoside Rg3 combined with cyclophosphamide on growth and angiogenesis of ovarian cancer

Background Ginsenoside Rg3, the main component isolated from ginseng, inhibits some kinds of tumour growth and angiogenesis. The combination of low dose chemotherapy and antiangiogenesis inhibitors suppresses growth of experimental tumours more effectively than conventional therapy. The effect of this combination on ovarian cancer remains to be evaluated. Therefore, we investigated the synergism of ginsenoside Rg3 and cyclophosphamide （CTX） on growth and angiogenesis of human ovarian cancer. Methods Twenty-eight female athymic mice were divided randomly into 4 groups of 7： ginsenoside Rg3, CTX, ginsenoside Rg3 and CTX combination and control, after being transplanted with ovarian cancer cells （SKOV-3）. The mice were given intraperitoneal injection of ginsenoside Rg3 and CTX for the 10 days following inoculation of SKOV-3 cells. The life quality and number of living days of mice were recorded. The size of tumour, tumour inhibitive rate, life elongation rate, proliferating cell nuclear antigen labelling index （PCNALI）, expression of vascular endothelial cell growth factor （VEGF） and microvessel density （MVD） of the tumour tissues were estimated. Results Life quality of mice in ginsenoside Rg3 and combined treatment groups were better and number of living days longer than control. Average tumour weights of each treated group were less than control and there was no significant difference among the treated groups. PCNALI of treated groups was lower than control. The MVD value and VEGF expression in treated groups were significantly lower than control and the MVD values of ginsenoside Rg3 and combined treatment groups were lower than that of CTX group. Conclusions Ginsenoside Rg3 significantly inhibited growth and angiogenesis of ovarian cancer when used alone or combined with CTX. Ginsenoside Rg3 and CTX combination reinforced the antitumour effect each other and improved the living quality and survival time of mice with tumour.     

Ginsenoside Rgl-induced alterations in gene expression in TNF-α stimulated endothelial cells

Background In China the ginseng root began to be used in medicine over 2000 years ago.Ginsenosides are the most important component isolated from ginseng. The authors investigated the effect of ginsenoside Rgl on the spectrum of gene expression in the endothelial cells stimulated by TNF-α and further explored the potential molecular mechanism of endothelial protection by ginsenoside Rgl.Methods Nitric oxide (NO) production in(HUVECs) was measured by using an NOthe cultured human umbilical vein endothelial cells assay kit. A home-made oligonucleotide microarray containing approximately 400 cardiovascular disease-related genes was constructed. The alteration of the spectrum of gene expression induced by ginsenoside Rgl in HUVECs which were activated by TNF-α were detected by oligonucleotide microarray analysis.Results NO production in HUVECs was decreased significantly after TNF-α treatment, while pretreatment with ginsenoside Rgl enhanced NO production in TNF-αstimulated HUVECs.Ginsenoside Rg1 affected the expression levels of genes involved in vascular constriction, cell adherence, coagulation, cell growth and signal transduction in TNF-αstimulated HUVECs.Conclusions Ginsenoside Rgl could enhance NO production and the expression of eNOS mRNA in TNF-α stimulated HUVECs. Ginsenoside Rgl regulated sets of genes in endothelial cells and protected endothelial cells from TNF-αectivation. Microarray analysis provided us with valuable insights into the atheroprotective mechanism by gingsenoside Rg1.     

反义血管内皮细胞生长因子基因转染在调节人肺巨细胞癌血管生成及肿瘤生长

OBJECTIVE: To study the regulatory effect of antisense VEGF121 cDNA transfection on endogenous VEGF secretion and angiogenesis of human metastatic lung carcinoma cell line PG and explore the significance of microvessel density (MVD) in tumor growth and metastasis. METHODS: The eukaryotic expression vectors bearing antisense VEGF121 cDNA was transfected into PG cells. Human umbilical vein endothelial cells (HUVEC) were cultured in conditioned mediums from transfected cells, and proliferation was determined by methyl thiazolyl tetrazolium (MTT) and 3H thymidine incorporation (3H TdR) assays in vitro. Microvessel density (MVD) in xenografted tumors in nude mice was analyzed by immunohistochemistry. RESULTS: The transfectant of antisense VEGF121 cDNA exhibited a reduction in VEGF secretion. HUVEC grown in conditioned medium from the antisense VEGF transfected cells exhibited a decrease in capacities of DNA syntheses and cell proliferation. MVD of tumor with transfected antisense VEGF gene was significantly lower than that in control vector. CONCLUSION: Antisense VEGF gene transfection can inhibit vascular endothelial cell proliferation in vitro and tumor angiogenesis in vivo, which may explain its inhibitory effects on tumor growth and metastasis.     

Ginsenoside Rg1-induced alterations in gene expression in TNF-α stimulated endothelial cells

Background In China the ginseng root began to be used in medicine over 2000 years ago. Ginsenosides are the most important component isolated from ginseng. The authors investigated the effect of ginsenoside Rg1 on the spectrum of gene expression in the endothelial cells stimulated by TNF-α and further explored the potential molecular mechanism of endothelial protection by ginsenoside Rg1.
Methods Nitric oxide (NO) production in the cultured human umbilical vein endothelial cells(HUVECs) was measured by using an NO assay kit. A home-made oligonucleotide microarray containing approximately 400 cardiovascular disease-related genes was constructed. The alteration of the spectrum of gene expression induced by ginsenoside Rg1 in HUVECs which were activated by TNF-α were detected by oligonucleotide microarray analysis.
Results NO production in HUVECs was decreased significantly after TNF-α treatment, while pretreatment with ginsenoside Rg1 enhanced NO production in TNF-αstimulated HUVECs. Ginsenoside Rg1 affected the expression levels of genes involved in vascular constriction, cell adherence, coagulation, cell growth and signal transduction in TNF-αstimulated HUVECs.
Conclusions Ginsenoside Rg1 could enhance NO production and the expression of eNOS mRNA in TNF-α stimulated HUVECs. Ginsenoside Rg1 regulated sets of genes in endothelial cells and protected endothelial cells from TNF-αactivation. Microarray analysis provided us with valuable insights into the atheroprotective mechanism by gingsenoside Rg1.
     

以神经内肽酶为靶点筛选治疗阿尔茨海默症天然药物的实验研究

目的筛选具有提高神经内肽酶(NEP)活性从而降低神经细胞β 淀粉样肽（Aβ）水平的药物,为临床治疗阿尔茨海默症（AD）提供实验依据。方法以脂质体LipofectamineTM2000介导瑞典突变型淀粉样肽前体蛋白(sweAPP)表达质粒pcDNA3.1 sweAPP转染神经母细胞瘤细胞SK N SH,G418筛选获得稳定表达细胞株作为AD模型细胞,采用蛋白印迹技术检测sweAPP表达情况,酶联免疫吸附试验（ELISA）检测细胞培养基中Aβ40和Aβ42含量变化,进而以MTT法检测各天然药物对SK N SH细胞增殖能力的影响,确定药物的有效浓度及最佳作用时间,以NEP肽酶实验检测药物对NEP酶活性影响,ELISA法检测药物对Aβ水平的影响。结果Western Blot结果显示,转染后SK N SH细胞高表达sweAPP蛋白;ELISA结果显示,转染后的SK N SH细胞分泌Aβ40、Aβ42明显升高,分别为转染前的7.26?和3.27倍（P<0.05）。NEP肽酶实验检测结果显示,茶多酚、人参皂苷Rb1、Rg3能够明显提高NEP酶活性,分别为（117±2.8）%、（131±4.0）%和（121±1.6）%。ELISA结果显示,经茶多酚、人参皂苷Rb1、Rg3作用后,细胞培养基中Aβ40和Aβ42水平明显降低,分别为对照组的（82±0.78）%和（85±2.21）%、（74±1.61）%和（99±3.31）%、（83±5.31）%和（76±6.74）%。结论成功构建AD模型细胞;茶多酚、人参皂苷Rb1、Rg3可提高NEP酶活性,从而有效降低Aβ的水平;本研究为茶多酚、人参皂苷Rb1、Rg3在临床上的应用以及分子机制研究提供了试验数据。     

人参皂苷Rg3对大鼠脑胶质瘤GFAP,Vimentin表达的影响

目的：观察人参皂苷Rg3对大鼠C6胶质瘤胶质纤维酸性蛋白（GFAP）、波形蛋白（Vimentin）表达的影响,探讨人参皂苷Rg3抗胶质瘤作用机制.方法：制备大鼠脑C6胶质瘤模型,实验分为人参皂苷Rg3溶媒混合物治疗组,溶媒组,生理盐水组,在接种细胞模型建立2wk后,人参皂苷Rg3溶媒混合物治疗组给予人参皂苷Rg3,4wk后处死大鼠并观察肿瘤形成情况,进行GFAP,Vimentin免疫组织化学检测并分析组间差异.结果：免疫组织化学染色显示GFAP,Vimentin在各组均表达.溶媒组和生理盐水组GFAP表达面密度值分别为（0.12±0.01）,（0.11±0.01）;光密度值分别为（692.80±146.38）,（647.54±127.62）.应用人参皂苷Rg3后,GFAP面密度值和光密度值表达明显增强,分别为（0.24±0.02）,（882.80±150.67）,差异具有统计学意义（P〈0.01）;溶媒组和生理盐水组Vimentin表达面密度值分别为（0.19±0.02）,（0.20±0.01）,光密度值分别为（792.80±131.28）,（817.54±137.62）.应用人参皂苷Rg3后,Vimentin面密度值和光密度值表达明显减弱,分别为（0.10±0.01）,（682.31±126.38）,差异具有统计学意义（P〈0.01）.而溶媒组与生理盐水组之间GFAP,Vimentin面密度值与光密度值表达差异无统计学意义.结论：人参皂苷Rg3可能是通过抑制脑胶质瘤Vimentin的表达,同时增强GFAP的表达以起到抗肿瘤的作用.     

反义血管内皮细胞生长因子基因转染在调节人肺巨细胞癌血管生成及肿瘤生长和转移中的作用

目的　探讨反义血管内皮细胞生长因子 (VEGF)基因转染在减少肿瘤细胞内源性血管内皮细胞生长因子分泌 ,调节肿瘤血管生成和肿瘤生长转移中的作用。方法　利用脂质体法将反义基因转染到高转移性人肺癌细胞 (PG) ,以转基因肿瘤细胞培养上清刺激人脐静脉内皮细胞 ,进行噻唑蓝 (MTT)和3H胸腺嘧啶 (3HTdR)掺入实验 ;并将转基因肿瘤细胞接种于裸鼠体内 ,应用免疫组织化学法检测肿瘤内微血管密度 (MVD) ,探讨MVD与肿瘤生长转移的关系。结果　反义VEGF基因的转染 ,使肿瘤细胞VEGF分泌减少 ,其培养上清刺激人脐静脉内皮细胞 (HUVEC)生长活性较空载体组减弱 ,HUVEC之DNA合成减少 ,裸鼠移植瘤内MVD为 41个± 9个 ,空载体组为 5 8个± 10个 ,两组比较t=2 715 ,P <0 .0 5。结论　反义VEGF基因的转染使肿瘤细胞分泌VEGF能力下降 ,肿瘤血管生成能力降低 ,这在肿瘤的生长和转移调节中有重要意义。     

人参皂甙Rg3在体外对胃癌细胞生长和凋亡的影响

目的 研究人参皂甙Rg3在体外对低、中分化胃腺癌细胞株MKN-45和SGC-7901生长及凋亡的影响。方法 取处于对数生长期的MKN-45和SGC-7901细胞,加入不同终浓度（20、30、40、50 μg/mL）的人参皂甙Rg3分别培养24、48 h或24、48和72 h,以不加药细胞作为阴性对照。MTT法检测MKN-45和SGC-7901细胞生长抑制率;流式细胞仪Annexin V/PI双染法检测SGC-7901细胞凋亡率;流式细胞仪分析SGC-7901细胞周期;透射电子显微镜观察50 μg/mL人参皂甙Rg3处理组SGC-7901细胞的形态学改变。结果 人参皂甙Rg3各处理组SGC-7901和MKN-45细胞生长抑制率均明显高于对照组(P<0.05),且随药物浓度的增加和作用时间的延长而上升(P<0.05)。与对照组比较,人参皂甙Rg3各处理组SGC-7901细胞凋亡率和G0/G1期细胞百分比均明显上升,且呈浓度和时间依赖性。透射电子显微镜观察50 μg/mL人参皂甙Rg3处理组SGC-7901细胞,可见典型的凋亡细胞结构。结论 人参皂甙Rg3在体外对胃癌细胞生长具有抑制作用,且呈现一定的时效和量效关系,其机制可能与诱导胃癌细胞凋亡有关。