珍珠舌草胶囊总黄酮苷对胃癌细胞AGS生长的影响及机制研究

目的:对珍珠舌草胶囊进行拆方研究,观察其总黄酮苷对胃癌AGS细胞增殖和凋亡的影响及其作用机制。方法:对珍珠舌草胶囊组成中药进行生药鉴定后,提取总黄酮苷;应用MTT法检测总黄酮苷及对胃癌细胞AGS生长的影响;应用流式细胞仪检测总黄酮苷对胃癌AGS细胞周期和细胞凋亡的影响;比色法测定药物对肿瘤细胞Caspase 3活性的影响;药物干预期间用显微镜观察细胞数量及形态学变化。结果:珍珠舌草胶囊总黄酮苷可明显抑制胃癌AGS细胞的生长,该作用呈时间与剂量依赖性。总黄酮苷可以阻滞细胞周期于G2/M期;还可以促进细胞的凋亡,显著增强Caspase 3的活性。结论:珍珠舌草胶囊总黄酮苷能显著抑制AGS细胞的增殖。阻滞细胞周期于G2/M期,并诱导和促进细胞凋亡。促凋亡作用可能通过Caspase 3的活性增强途径实现。     

多伞阿魏体外抗胃癌活性筛选、细胞凋亡及周期阻滞机制

目的:研究确定新疆特色维族药多伞阿魏体外抗胃癌活性部位及其敏感胃癌细胞系,并探讨多伞阿魏诱导胃癌细胞凋亡和细胞周期阻滞情况,为其进一步在抗胃癌方面的研究、开发与应用提供实验依据。方法:采用四甲基偶氮唑盐(MTT)比色法检测不同质量浓度多伞阿魏不同提取物(挥发油,95%乙醇提取物,及其石油醚部位,三氯甲烷部位,乙酸乙酯部位,正丁醇部位,水部位)分别对5种胃癌细胞系(AGS,MKN-45,BGC-823,MGC-803,SGC-7901)的增殖抑制作用;采用Hoechst33258荧光染色法观察多伞阿魏挥发油和三氯甲烷部位对胃癌细胞AGS和SGC-7901的影响情况;并应用细胞流式仪检测多伞阿魏不同提取部位作用胃癌细胞AGS和SGC-7901的凋亡和周期阻滞影响情况。结果:与空白组比较,多伞阿魏挥发油,95%乙醇提取物,石油醚部位,三氯甲烷部位,乙酸乙酯部位对5种胃癌细胞均有不同程度的增殖抑制作用(P0.05),并呈现浓度依赖关系。挥发油对胃癌细胞AGS呈现出较强的增殖抑制作用,其半数抑制浓度(IC50)为(7.98±2.62)mg·L~(-1),三氯甲烷部位对5种胃癌细胞系均具有较好的敏感性,对胃癌细胞SGC-7901最为敏感,其IC50为(8.73±0.55)mg·L~(-1),而正丁醇部位和水部位未呈现出明显的细胞增殖抑制作用;多伞阿魏挥发油和三氯甲烷部位作用胃癌细胞AGS和SGC-7901后,细胞核被Hoechst33258染色呈亮蓝色,且随着药物浓度的增加蓝色荧光越强;流式细胞凋亡检测结果显示,多伞阿魏不同提取部位诱导胃癌细胞AGS和SGC-7901发生不同程度的凋亡(P0.05),且随着药物浓度的增加,细胞总凋亡率明显增高;流式细胞周期检测结果显示,与空白组比较,多伞阿魏挥发油使胃癌细胞AGS的周期发生明显改变,细胞休眠期/DNA复制前期(G0/G1期)细胞比例增高,DNA复制期(S期)细胞比例降低,DNA复制后期/有丝分裂期(G2/M期)比例降低(P0.05);与空白组比较,多伞阿魏三氯甲烷部位使胃癌细胞SGC-7901的周期也发生显著改变,G0/G1期细胞比例降低,S期细胞比例增高,G2/M期比例降低(P0.05)。结论:多伞阿魏挥发油对胃癌细胞AGS呈现出较强的细胞毒活性,三氯甲烷部位对5种胃癌细胞均具有较好的增殖抑制作用,尤其对胃癌细胞SGC-7901最为敏感;多伞阿魏各提取部位诱导胃癌细胞AGS和SGC-7901主要发生晚期凋亡,而多伞阿魏乙酸乙酯部位诱导胃癌细胞AGS主要发生细胞早期凋亡;多伞阿魏挥发油能够将胃癌细胞AGS阻滞于G0/G1期,阻止细胞进入S期及G2/M期;伞阿魏三氯甲烷部位将胃癌SGC-7901细胞周期阻滞于S期。研究表明多伞阿魏挥发油和三氯甲烷部位具有较好的抗胃癌活性作用,具有潜在的研究价值和开发利用空间,并为多伞阿魏体内抗胃癌及其抗胃癌机制研究提供了一定的科学依据。     

丹参素对胃癌AGS细胞凋亡的影响及其机制研究

目的：研究丹参素对人胃腺癌AGS细胞凋亡的影响及其机制。方法：将人胃腺癌AGS细胞在体外培养至其生长良好后用不同浓度的丹参素处理AGS细胞24 h、48 h,用CCK8、流式细胞仪、Western blotting法检测丹参素对AGS细胞增殖抑制、凋亡、周期和蛋白表达的影响。结果：与空白组比较,丹参素作用于AGS细胞后对其生长起着抑制作用（P<0.05）,具有时间和浓度依赖关系;且可促进细胞凋亡（P<0.05）,阻滞细胞于G2/M期（P<0.05）;促进p53、Cytochrome C、Bax蛋白表达（P<0.05）,抑制BCL-2蛋白表达（P<0.05）。结论：丹参素能够抑制胃癌AGS细胞的生长,促进AGS细胞凋亡,其机制与丹参素阻滞细胞于G2/M期、启动线粒体凋亡有关。     

鸦胆子油乳抑制胃癌细胞增殖及其机制的研究

目的研究鸦胆子油乳体外对人胃癌细胞BGC-823抑制增殖的作用及对细胞周期、细胞凋亡及p53表达的影响．探讨其抗肿瘤机制。方法：MTT法检测鸦胆子油乳对BGC-823细胞的毒性作用：漉式细胞仪检测细胞凋亡和细胞周期分布；免疫细胞化学染色检测p53表达。结果：鸦胆子油乳对人胃癌细胞有显著的增殖抑制作用，且有时间和浓度依赖性：0．10g/L鸦胆子油乳作用12、24、48h后，凋亡率明显上升，细胞周期被阻滞于G0／G1期；p53表达水平增高。结论：鸦胆子油乳体外对胃癌细胞BGC-823有显著的抑制增殖作用，上调p53的表达从而能诱导凋亡、阻滞细胞周期于C0／C1期是其重要机制。     

胃复春胶囊通过调节Bcl-2/Bax号通路诱导胃癌细胞凋亡

目的 研究胃复春胶囊对人胃癌细胞的作用,为胃复春胶囊在抗消化道肿瘤方面的应用提供依据。方法 NCI-N87人胃癌细胞与不同浓度的胃复春胶囊提取物共孵育,采用Cell Counting Kit-8试剂盒检测细胞活力;流式细胞术Annexin V/PI双染色检测细胞凋亡及细胞周期;Western blot法检测与细胞凋亡相关的蛋白表达情况。结果 胃复春胶囊提取物能够剂量和时间依赖地抑制NCI-N87细胞生长,诱导NCI-N87细胞产生凋亡,且使细胞周期阻滞在G0/G1期;经过胃复春胶囊提取物处理24 h后,实验组NCI-N87细胞中抗凋亡蛋白Bcl-2、Bcl-w表达量下调;促凋亡蛋白Bax、Bad表达量上调,呈剂量依赖性。结论 胃复春胶囊提取物能抑制胃癌细胞的增殖、阻滞细胞周期并诱导细胞凋亡,其作用机制推测与Bcl-2/Bax信号通路有关。文章为临床上胃复春胶囊治疗胃癌提供了依据。     

姜黄素对人胃癌AGS细胞自噬流的作用

目的探讨姜黄素对人胃癌AGS细胞自噬流的作用。方法 5、10、20μmol/L浓度的姜黄素处理AGS细胞24 h,采用MTT法观察姜黄素对AGS胃癌细胞增殖的抑制作用,Western blot检测姜黄素对微管相关蛋白LC3和泛素相关蛋白SQSTM1/p62蛋白表达的影响。Western blot检测自噬抑制剂氯喹与姜黄素联合使用对LC3和SQSTM1/p62蛋白表达的影响。结果 MTT结果显示,姜黄素可以明显抑制AGS胃癌细胞的增殖,并且呈剂量依赖性(P0.05,P0.01)。Western blot结果显示,随着姜黄素浓度的增加,LC3-Ⅱ和SQSTM1/p62蛋白的表达均呈剂量依赖地上调(P0.05,P0.01),提示姜黄素可以引起自噬体的堆积。自噬抑制剂氯喹与姜黄素联合使用可以增强LC3-Ⅱ和SQSTM1/p62蛋白表达的上调,进一步验证了姜黄素对自噬流的抑制作用。结论姜黄素可能通过阻滞人AGS胃癌细胞自噬体降解,抑制AGS胃癌细胞的自噬流,促进AGS胃癌细胞的死亡。     

茅苍术提取物对胃癌BGC-823和SGC-7901细胞增殖抑制作用研究

目的探讨茅苍术提取物对胃癌细胞株BGC-823和SGC-7901的增殖抑制效应。方法采用不同浓度(0.625,1.25,2.55,10 mg.mL-)1茅苍术水提物处理胃癌BGC-823和SGC-7901细胞,采用四甲基偶氮唑盐(MTT)法检测药物对细胞的抑制作用;倒置显微镜下观察细胞的形态学改变;Hoechst 33342染色,荧光显微镜观察细胞凋亡形态;应用流式细胞仪观察凋亡过程中的细胞周期变化。结果茅苍术提取物对胃癌BGC-823和SGC-7901细胞增殖均有明显的抑制作用,且呈浓度和时间依赖性;光镜下可见凋亡细胞的形态学特征性改变;流式细胞仪检测表明经茅苍术提取物处理,BGC-823细胞周期阻滞于S期,SGC-7901细胞周期阻滞于G0/G1期。结论体外实验显示茅苍术提取物能抑制胃癌BGC-823和SGC-7901细胞增殖,可以诱导胃癌细胞凋亡。     

蜂斗菜素对人胃癌SGC7901细胞增殖抑制和诱导凋亡作用

目的观察蜂斗菜素对人胃癌细胞SGC7901增殖及凋亡影响,并探讨其作用机制。方法磺酰罗丹明B(Sulforhodamine B,SRB)法检测细胞增殖抑制作用,流式细胞术检测细胞凋亡及周期阻滞,免疫印迹法(Western blot)检测肿瘤抑制基因p53蛋白的表达及细胞外信号调节激酶1/2(ERK1/2)磷酸化水平。结果蜂斗菜素作用24、48、72 h后对人胃癌SGC7901细胞均有显著的增殖抑制作用,并具有剂量和时间依赖性;与对照组相比,蜂斗菜素作用48 h后G_1/G0期细胞比率增加,S期及G_2/M期细胞比率下降,细胞凋亡率升高;和对照组相比,蜂斗菜素作用48 h后,细胞中p53蛋白表达显著增加增加,ERK1/2磷酸化水平则显著降低。结论蜂斗菜素对人胃癌SGC7901细胞具有增殖抑制、细胞周期阻滞及诱导凋亡作用,其机制可能与增加p53蛋白表达和降低ERK1/2磷酸化水平有关。     

白藜芦醇诱导胃癌细胞脱落凋亡

目的 研究白藜芦醇诱导胃癌细胞脱落凋亡的作用。方法 采用细胞形态学观察、Annxin-V和PI细胞染色和流式细胞仪检测，观察白藜芦醇(0．1、0．2、0．5 mmol／L)对脱落培养胃癌细胞BGC823、SGC7901和HGC27的生长状态、细胞周期的影响及诱导脱落凋亡的作用。结果 倒置显微镜下发现脱落培养的胃癌细胞聚集成团生长，0．1mmol／L白藜芦醇作用细胞后可抑制抗脱落凋亡的胃癌细胞聚集成团；流式细胞仪检测和Annxin-V和PI细胞染色表明0．5mmol／L白藜芦醇可分别阻滞脱落培养的BGc823、sGc7901和HGc27细胞于G0／G1、S、G2／M期，并可诱导这3株胃癌细胞发生脱落凋亡，其中自藜芦醇诱导HGC27细胞脱落凋亡比例达19．3％，远高于其他两株胃癌细胞。结论自藜芦醇可诱导胃癌细胞发生脱落凋亡。     

鬼臼毒素诱导胃癌细胞株SGC-7901凋亡的实验研究

目的:研究鬼臼毒素诱导胃癌细胞株SGC-7901凋亡,为鬼臼毒素用于临床治疗胃癌提供依据。方法:用不同浓度的鬼臼毒素处理SGC-7901细胞后,采用MTT比色法检测其对SGC-7901细胞增殖的抑制作用;采用流式细胞术检测细胞周期分布和细胞的凋亡率;用Hoechst 33258染液染色,在荧光显微镜下观察细胞凋亡形态。结果:鬼臼毒素可以抑制SGC-7901细胞增殖,呈剂量依赖性。能够诱导SGC-7901细胞凋亡,并使SGC-7901细胞阻滞于G2/M期,细胞凋亡率呈剂量依赖性。通过荧光显微镜可以明显的观察到凋亡小体。结论:鬼臼毒素能抑制胃癌SGC-7901细胞的增殖,诱导SGC-7901细胞凋亡,此为鬼臼毒素临床治疗胃癌提供了科学依据。     

橙皮苷诱导人胃癌AGS细胞凋亡机制的研究

目的探讨橙皮苷对胃癌AGS细胞的诱导凋亡作用及其相关分子机制。方法采用MTT比色法检测橙皮苷对AGS细胞的杀伤作用;Annexin V-FITC/PI双染法和流式细胞术检测橙皮苷对AGS细胞的诱导凋亡作用、活性氧水平及加入活性氧清除剂N-乙酰-L-半胱氨酸(NAC)后细胞凋亡变化情况;Western blotting法检测细胞凋亡相关蛋白和丝裂原活化蛋白激酶(MAPK)信号通路相关蛋白的表达。结果 MTT比色法检测结果显示橙皮苷对AGS具有良好的增殖抑制作用。经橙皮苷处理后AGS细胞呈现细胞核固缩、细胞皱缩等凋亡现象。Annexin V-FITC/PI双染法和流式细胞术检测结果表明橙皮苷可以诱导AGS细胞发生线粒体依赖性凋亡,增加细胞内活性氧的水平,预处理NAC后,橙皮苷的诱导凋亡作用被抑制。Western blotting检测结果显示p-JNK、p-p38、Bad、cleavedCaspase-3及活化的聚腺苷二磷酸核糖聚合酶(cleavePARP)蛋白表达水平升高,抗凋亡蛋白磷酸化细胞外调节蛋白激酶(p-ERK)及Bcl-2表达水平降低,说明橙皮苷激活了AGS细胞中的MAPK信号通路及线粒体依赖性凋亡。结论橙皮苷对AGS细胞具有良好的杀伤作用,并通过提高AGS细胞内活性氧水平,进而调控MAPK信号通路来诱导AGS细胞发生线粒体依赖性凋亡。     

Induction of G2/M arrest and apoptosis by water extract of Strychni Semen in human gastric carcinoma AGS cells

The seed of Strychnos nux-vomica (Loganiaceae) has been used in traditional Oriental medicine as a folk remedy for the treatment of cancer. However, the mechanism responsible for the anticancer effects of Strychni Semen is not clearly understood. The study tested whether and how the water extract of Strychni Semen (ESS) treatment would affect the growth of AGS human gastric carcinoma cells. ESS was found to inhibit the growth of AGS cells in a concentration-dependent manner. Cell cycle analysis showed G2/M phase arrest and apoptosis in AGS cells following ESS treatment. ESS-mediated G2/M arrest was found to be associated with up-regulation of cyclin A, Cdc2, tumor suppressor p53 and cyclin dependent kinase (Cdk) inhibitor p21(WAF1/CIP1), whereas the expressions of other G2/M regulatory proteins, including cyclin B1 and Cdk2, were down-regulated compared with the control. The induction of apoptotic cell death by ESS was associated with down-regulation of anti-apoptotic Bcl-2 and up-regulation of pro-apoptotic Bax expression. Further results indicate that caspase-3, caspase-8 and caspase-9 are all activated by ESS, together with cleavage of downstream caspase-3 target proteins. Taken together, the results of this study suggest the involvement of multiple signaling pathways targeted by ESS in mediating G2/M cell cycle arrest and apoptosis in AGS cells, and warrant further investigation.     

Astragalus saponins modulate cell invasiveness and angiogenesis in human gastric adenocarcinoma cells

Aim of the study

We had reported that Astragalus saponins (AST) exert promising anti-tumorigenic effects by suppressing the growth of HT-29 human colon cancer cells and tumor xenograft. In the present study, we further investigated the anti-angiogenic property of AST in human gastric adenocarcinoma cells (AGS) and attempted to elucidate the underlying mechanism.

Materials and methods

Viability of AGS cells was measured by using the MTT reduction method. Western blotting was performed to examine the effect of AST on apoptotic- and cell growth-related protein expression. Effect of AST on cell cycle progression was also evaluated using PI staining. A Matrigel invasion assay was then employed to demonstrate the effect of AST on the invasiveness of gastric cancer cells. The expression of invasion-associated proteins (VEGF and MMPs) was also investigated.

Results

AST could induce apoptosis in AGS cells by activating caspase 3 with subsequent cleavage of poly(ADP-ribose) polymerase. Besides, cell cycle arrest at the G2/M phase had been observed in AST-treated cells, leading to substantial growth inhibition. The anti-proliferative effect of AST was associated with the regulation of cyclin B1, p21 and c-myc. Results indicate that the number of AGS cells invaded through the Matrigel membrane was significantly reduced upon AST treatment, with concomitant down-regulation of the pro-angiogenic protein vascular endothelial growth factor (VEGF) as well as the metastatic proteins metalloproteinase (MMP)-2 and MMP-9.

Conclusion

AST derived from the medicinal plant Astragalus membranaceus could modulate the invasiveness and angiogenesis of AGS cells besides its pro-apoptotic and anti-proliferative activities. These findings also suggest that AST has the potential to be further developed into an effective chemotherapeutic agent in treating advanced and metastatic gastric cancers.     

Sangre de grado Croton palanostigma induces apoptosis in human gastrointestinal cancer cells

Sangre de grado is an ethnomedicinal red tree sap obtained from Croton spp. that is used to treat gastrointestinal ulcers, cancer and to promote wound healing. To evaluate the potential role of sangre de grado (SdG) in cancer we examined its effects on human cancer cells, AGS (stomach), HT29 and T84 (colon). Viability of cells treated with SdG (10–200 μg/ml) decreased (P<0.01) in a dose dependent manner measured over a 24-h period. Cell proliferation at 48 h decreased (P<0.01) in all cells treated with SdG (>100 μg/ml). When cells in suspension were treated with SdG (100 μg/ml) cell adherence was severely compromised (>85%). Cells treated with SdG (100 μg/ml) underwent apoptosis as detected by nucleus condensation and DNA fragmentation determined by ELISA, and flow cytometry. Morphological changes as assessed by acridine orange. These effects were similar to that observed with Taxol (30 μM). A significant alteration of microtubular architecture was equally observed in both stomach and colon cancer cells exposed to SdG (100 μg/ml). The induction of apoptosis and microtubule damage in AGS, HT29 and T84 cells suggest that sangre de grado should be evaluated further as a potential source of anti-cancer agents.     

右旋柠烯对不同类型人胃癌细胞的生长抑制作用

目的：探讨右旋柠烯(D-limonene)对不同类型人胃癌细胞的生长抑制作用及其机制。方法：以D-limonene作用于SGC-7901、BGC-823及AGS三种不同类型人胃癌细胞，采用噻唑蓝(MTT)比色法、流式细胞仪及电镜检测细胞生长抑制率、凋亡率以及形态学改变，免疫细胞化学法检测p53、bax和bcl-2基因表达。结果：D-limonene处理后的细胞生长抑制率与凋亡率均增加，与药物浓度呈正相关。细胞呈现核固缩、染色质边集、凋亡小体形成等典型凋亡表现。经D-limonene处理后SGC-7901、BGC-823细胞株p53、bax蛋白表达明显增加，bcl-2蛋白表达降低。AGS细胞株bax蛋白表达明显增加，bcl-2蛋白表达降低。结论：D-limonene对人胃癌细胞的抑制作用主要是通过诱导细胞凋亡，不同类型的细胞株作用途径可能不同。升提p53与bax及降低bcl-2的蛋白表达为其诱发冒癌细胞．凋亡的机制之一。     

青蒿酿液体外抗肿瘤活性研究

目的研究青蒿酿液的体外抗肿瘤活性。方法采用四甲基偶氮唑盐法测定青蒿酿液体外抑制人肺癌A549、MDA231细胞,结肠癌SW620、LOVO细胞,胃癌AGS细胞以及肝癌Hep-2细胞的活性。结果青蒿酿液对以上六株肿瘤细胞均有明显的抑制作用。结论青蒿酿液在体外对人肺癌A549、MDA231细胞,结肠癌SW620、LOVO细胞,胃癌AGS细胞以及肝癌Hep-2细胞均有明显的抗肿瘤作用。     

Inhibition of Helicobacter pylori-induced inflammation in human gastric epithelial AGS cells by Phyllanthus urinaria extracts

AIM OF THE STUDY: Helicobacter pylori is linked to a majority of peptic ulcers and to some types of gastric cancer, and its resistance to antibiotic treatment is now found worldwide. This study is aimed at evaluating the antimicrobial activity of Phyllanthus urinaria Linnea (Euphorbiaceae), chloroform (PUC) and methanol (PUM) extracts, and its eight isolates on H. pylori-infected human gastric epithelial AGS cells. MATERIALS AND METHODS: The in vitro anti-bacterial activity of P. urinaria chloroform (PUC) and methanol (PUM) extracts, and its eight isolates were determined. Additional experiments were also performed to know the PUC and PUM ability to inhibit the H. pylori adhesion to and invasion of AGS cells, in addition to the effect of PUC on NF-kappaB activity as well as IL-8 synthesis during H. pylori infection of AGS cells. RESULTS: The results revealed that crude extracts PUC and PUM showed potent antimicrobial activity against H. pylori than pure isolates. On the other hand, in vitroH. pylori-infection model revealed that the inhibition of bacterial adhesion and invasion to AGS cells has dramatically reduced by treatment of extract PUC, while PUM has the same moderate effect. Furthermore, H. pylori-induced nuclear factor (NF)-kappaB activation, and the subsequent release of interleukin (IL)-8 in AGS cells were also inhibited by the extract PUC. CONCLUSIONS: These results open the possibility of considering P. urinaria a chemopreventive agent for peptic ulcer or gastric cancer, but this bioactivity should be confirmed in vivo in the future.     

常用14种抗肿瘤中药体外抑瘤效果比较

目的:比较14种常用抗肿瘤中药的体外抑瘤效果。方法:采用四甲基偶氮唑兰(MTT)法分别测定了14种常用抗肿瘤中药的水提液、醇提液对人胃癌细胞株AGS、人胃癌细胞株BGC-823体外增殖反应的影响。结果:该14种中药中有10味体外对人胃癌细胞株AGS、人胃癌细胞株BGC-823体外增殖均有阳性抑制作用;且该10味中药醇提液体外对人胃癌细胞株AGS、人胃癌细胞株BGC-823体外增殖抑制作用优于水提液;有2味中药醇提浸膏对人胃癌细胞株AGS、人胃癌细胞株BGC-823体外增殖抑制作用均为强阳性;而其余2味中药对2株细胞抑制率为阴性。结论:14种中药中10味体外对胃癌细胞抑制率大于50%,但提取工艺对抑瘤效果存在较大影响,应尽量采用醇提工艺提取。     

基于ZEB2、14-3-3ζ/TGF-β/smad通路探讨七方胃痛颗粒对人胃腺癌AGS细胞EMT的影响

目的探讨七方胃痛颗粒对ZEB2、14-3-3ζ/TGF-β/smad通路介导胃癌EMT和获得浸润侵袭转移能力过程中的作用和机制及对EMT细胞的ZEB2、14-3-3ζ表达的影响,为七方胃痛颗粒防治胃癌提供理论依据。方法参照血清药理学方法制备七方胃痛颗粒含药血清,观察七方胃痛颗粒中药对AGS细胞、TGF-β1诱导AGS细胞形成EMT细胞的干预情况,分别采用细胞划痕试验、Transwell细胞侵袭试验和MTT法检测细胞侵袭迁移穿透能力;采用Western Blot、RT-PCR法检测细胞ZEB2、14-3-3ζ的转录及表达情况。结果与TGF-β1/Smad组和空白对照组相比,七方胃痛颗粒能抑制人胃腺癌AGS细胞及EMT细胞的增殖、侵袭和穿透能力(P<0.05),且EMT细胞中ZEB2、14-3-3ζ蛋白和mRNA表达降低(P<0.05),并呈时间依赖性。结论在体外试验中,七方胃痛颗粒能抑制人胃腺癌AGS细胞及其EMT细胞的增殖、侵袭和穿透能力,其机制可能与抑制其ZEB2、14-3-3ζ及TGF-β/smad通路相关,从而达到抗癌作用。