Inhibitory Effect of α-Pinene on SGC-7901 Cell Proliferation and the Mechanism of ATM Kinase Signaling Pathway

Objective: To research the inhibitory effect on SGC-7901 cells of α-pinene, and the related mechanism of α-pinene. Methods: Used the MTT method to detect inhibition rate and western blotting to detect the influence on expression of ATM, Phos-S1981ATM, H2AX, γH2AX, CHK2 and p-CHK2, p53 and phos-p53 cell cycle related protein in SGC-7901 cells. Results: The research found α-pinene could inhibit the proliferation of SGC-7901 cells observably in vitro, and the inhibition rate assumes the dependence on concentration;and western blotting results showed that, α-pinene could activate phospho-ATM, increase the amount of γH2AX (p p < 0.05);increase the expression of p-CHK2, p53 and phos-p53 (p p p < 0.05);But there is no significant effect on expression of CHK2 (p > 0.05). Conclusions: α-pinene could inhibit the proliferation of SGC-7901 cells, and by inducing ATM (Ataxia Telangiectasia-Mutated) kinase signal pathway in DNA damage response, activating cell cycle checkpoint, making the cell cycle arrest then exerts its anti-tumor effects.

Inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 in vitro and in vivo

AIM:To investigate the inhibitory effect of acetylshikonin on human gastric carcinoma cell line SGC-7901 and its mechanism. METHODS:MTT assay was used to assess the inhibitory effect of acetylshikonin on proliferation of SGC-7901 cells.Apopt osis-inducing effect was determined by flow cytometry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling with Hoechst staining.Expression of mRNA and protein in Bcl-2 and Bax was analyzed by reverse transcription-polymerase chain reaction and Western blot.Antitumor effect of acetylshikonin on a mouse SGC-7901 model was also determined. RESULTS:Forty-eight hours after treatment with acetylshikonin,MTT assay showed that acetylshikonin inhibited the proliferation of SGC-7901 cells in a dose-dependent manner.The half maximal inhibitory concentration of acetylshikonin to SGC-7901 cells was 0.428±0.07 mg/L.Cell shrinkage,nuclear pyknosis and chromatin condensation,which are the characteristics of cell apoptosis,were observed in treated SGC-7901 cells and the percentage of apoptosis increased in a dose-dependent manner.Acetylshikonin downregulated the expression of Bcl-2 and up-regulated the expression of Bax in the treated SGC-7901 cells compared with the controls.The experiment in vivo showed that 0.5,1,and 2 mg/kg of acetylshikonin significantly inhibited the growth of tumor in the mouse SGC-7901 model,with an inhibitory rate of 25.00%-55.76%. CONCLUSION:Acetylshikonin inhibits the growth of SGC-7901 cells in vitro and in vivo by inducing cell apoptosis.

Growth inhibitory effect of 4-phenyl butyric acid on human gastric cancer cells is associated with cell cycle arrest

AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated MGC-803 cells were treated with 5, 10, 20, 40, and 60 μmol/L PBA for 1-4 d. Cell proliferation was detected using the MTT colorimetric assay. Cell cycle distributions were examined using flow cytometry.RESULTS: The proliferation of gastric carcinoma cells was inhibited by PBA in a doseand time-dependent fashion. Flow cytometry showed that SGC-7901 cells treated with low concentrations of PBA were arrested at the G0/G1 phase, whereas cells treated with high concentrations of PBA were arrested at the G2/M phase. Although MGC-803 cells treated with low concentrations of PBA were also arrested at the G0/G1 phase, cells treated with high concentrations of PBA were arrested at the S phase. CONCLUSION: The growth inhibitory effect of PBA on gastric cancer cells is associated with alteration of the cell cycle. For moderately-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and G2/M phases. For lowly-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and S phases.

沙樱桃黄酮对SGC-7901细胞增殖的抑制作用

给予体外培养SGC-7901细胞沙樱桃黄酮,用克隆形成法和X射线能量色散谱仪,测定对细胞分裂增殖和细胞内微量元素含量的影响.结果表明,沙樱桃黄酮(0.1,0.5,5 mg.L-1)组和5-FU组克隆数比对照组明显减少,抑制率分别为27.60%、44.50%、66.60%和40.80%;细胞内Ca2+离子水平随给药浓度的增加而升高,K1+和P3+离子浓度则降低.

外源性三磷酸腺苷对人胃腺癌SGC-7901细胞的生物学效应

本文报道外源性三磷酸腺苷(ATP)对人胃腺癌SGC-7901细胞系增殖的抑制效应。在SGC-7901细胞的培养基质内加入ATP后,细胞生长明显受阻抑,4天以后,抑制率可达80%以上;癌细胞质膜上的3′,5′环腺苷酸磷酸二酯酶(cAMP-PDEase)活性明显下降,而细胞内的cAMP和纤维粘连蛋白的免疫荧光强度却明显增强。癌细胞多呈梭形,微绒毛减少,表面较光滑,呈现癌细胞向正常方向逆转的表型特征。本文还就ATP作用的机理进行了讨论。

黄芩苷抑制胃癌细胞SGC-7901增殖及机制研究

目的研究黄芩苷对人胃癌细胞SGC-7901增殖抑制作用及分子机制研究。方法将细胞随机分为对照组,3个浓度(50,100,200μmol·L^(-1))黄芩苷组,噻唑蓝法检测细胞活力;流式细胞术检测细胞周期;分光光度法检测细胞中天冬氨酸蛋白水解酶(Caspase 3)活性;免疫印迹法分析细胞周期蛋白(Cyclin A1)、Cyclin D1、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)蛋白含量表达及磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)通路的激活状况。结果与对照组比较,3个浓度黄芩苷可显著抑制SGC-7901细胞活力(P<0.05),上调Bax表达,而下调Bcl-2、Cyclin D1表达及AKT磷酸化水平(P<0.05),使SGC-7901细胞周期阻滞在G1期(P<0.05),并提高Caspase 3活性(P<0.05)。100,200μmol·L^(-1)黄芩苷可显著抑制Cyclin A1及PI3K表达量。结论黄芩苷可通过阻断PI3K/AKT信号通路的激活及下游相关分子的表达,进而抑制胃癌SGC-7901细胞增殖。

半夏总生物碱对人胃癌细胞增殖的抑制作用

目的观察半夏总生物碱(total alkaloids from Pinellia Ternate,TATP)对人胃癌细胞株SGC-7901增殖抑制的影响,探讨其可能的作用机制。方法采用四甲基偶氮唑盐比色法及集落形成率实验,检测不同浓度的TATP对SGC-7901细胞株的生长抑制作用;应用单细胞凝胶电泳技术检测TATP导致SGC-7901细胞的DNA损伤情况。结果人胃癌细胞SGC-7901经TATP处理后,其体外增殖能力明显下降,且与药物的剂量、干预时间呈正相关,与对照组比较,差异均有统计学意义(P<0.05或<0.01)。单细胞凝胶电泳(single cell gel electrophoresis,SCGE)中,TATP组细胞尾DNA含量、尾长及尾动量与对照组比较差异均有统计学意义(P<0.01),且呈现一定的浓度依赖性。结论一定剂量的TATP能明显抑制SGC-7901细胞的增殖,其作用机制可能与细胞DNA的损伤有关。

苍耳子药物血清对人肝癌细胞增殖的抑制作用

给予体外培养人肝癌细胞苍耳子药物血清,用克隆形成法和流式细胞仪检测对细胞分裂增殖和细胞凋亡的影响。结果表明,苍耳子药物血清(设低、中、高剂量)组和5-FU(5-氟尿嘧啶)组克隆数比对照组克隆数明显减少,克隆形成抑制率分别为18.30%、49.34%、68.12%和53.27%;苍耳子药物血清(低、中、高剂量)组和5-FU组细胞凋亡率分别为:6.1%、8.2%、16.3%和11.3%。苍耳子药物血清对人肝癌细胞分裂增殖具有明显的毒性和抑制作用。

人参皂苷Rh2及细胞因子诱导的杀伤细胞对人胃癌细胞株SGC-7901的体外增殖抑制作用

目的研究人参皂苷Rh2、细胞因子诱导的杀伤(CIK)细胞及二者联合对胃癌细胞株SGC-7901的体外增殖抑制作用。方法本试验采用MTT法检测30、35、40及45μg/ml人参皂苷Rh2以及效靶比分别为5:1、10:1、20:1和40:1的CIK细胞,35μg/ml的人参皂苷Rh2联合效靶比20:1的CIK细胞,分别作用于SGC-7901细胞24 h和48 h的增殖抑制作用。结果不同剂量的人参皂苷Rh2作用于SGC-7901细胞,在相同作用时间内,抑制率随着剂量的增加而增加,差异有统计学意义(P<0.01);随给药时间的延长,除45μg/ml组外,其他各剂量组作用48 h的抑制率均较24 h有显著上升,差异有统计学意义(P<0.05或0.01)。不同效靶比的CIK细胞作用于SGC-7901细胞后,在相同作用时间内,抑制率随着效靶比的增加而增加,差异有统计学意义(P<0.01);相同效靶比条件下,抑制率随着作用时间的延长而增加,差异均具有统计学意义(P<0.01)。35μg/ml的人参皂苷Rh2联合20:1的CIK细胞对SGC-7901细胞的增殖抑制作用显著强于人参皂苷Rh2或CIK细胞单用,差异均具有统计学意义(P<0.05或0.01)。结论人参皂苷Rh2及CIK细胞在体外对胃癌细胞株SGC-7901均具有一定增殖抑制作用,且在一定的条件下二者联合应用具有协同效果,较单用具有更强的抑制SGC-7901细胞增殖的作用。

蛇毒复合酶对人胃癌细胞的抑瘤研究

目的 观察蛇毒复合酶对人胃癌细胞 SGC-790 1的抑瘤作用及机理。 方法 采用体外试验、流式细胞术和细胞形态学检查方法 ,观察人胃癌细胞的生长抑制率 ,以及细胞周期和细胞形态的变化。 结果 蛇毒复合酶对人胃癌细胞有明显的抑瘤作用 ,2 4 h抑瘤率达 6 7.5 % ,接近 5 -Fu阳性对照组 ,并且具有明显的时效和量效关系。细胞镜检及涂片染色发现癌细胞胞膜破裂、胞质外溢、细胞坏死。流式细胞术检测蛇毒复合酶对 S期细胞有明显杀伤作用 ,同时阻滞 G0 / G1期细胞进入 S期。 结论 蛇毒复合酶对人胃癌细胞具有一定体外抑瘤作用 ,其作用机理与直接破坏细胞胞膜和干扰细胞增殖周期有关。

复方丹参药物血清对人胃癌细胞增殖的抑制作用

目的探讨复方丹参药物血清对入胃癌细胞增殖的抑制作用。方法给予体外培养人胃癌细胞复方丹参药物血清,用克隆形成法和流式细胞仪检测对细胞分裂增殖和细胞凋亡的影响。结果复方丹参药物血清(3.6、7.3、15g/kg)和5-氟脲嘧啶(5-FU)组克隆数比对照组克隆数(78.67±2.2)明显减少,克隆形成抑制率分别为13.1%、46.6%、64.0%和40.7%.复方丹参药物血清(3.6、7.3、15g/kg)组和5-FU凋亡率比对照组凋亡率(7.4%)明显增加,分别为:16.3%、24.2%、31.1%和22.1%。结论复方丹参药物血清对人胃癌细胞分裂增殖具有明显的毒性和抑制作用。