Objective To study the inhibitory effect of Acanthopanax giraldii Harms Var. Hispidus H oo polysaccharides (AGP) on SGC-7901 gastric cancer cells and its possible m echanism. Methods Cell doubling time analysis, colony forming assay and MTT assay were adopted to study the inhibitory effect and its characteristics. We also analyzed the amou nt of protein expressed by oncogenes, antioncogenes and cell factors using flow cytometric analysis.Results AGP inhibited the proliferation of SGC-7901 cells and cell colony forming abili ty. AGP did not inhibit the viability and function of lymphocytes of periphera l blood in healthy subjects and human embryonic tenocytes, except for the highes t dosage of AGP (P<0.05), which slightly inhibited the viability and functi on of the two types of normal cells. AGP inhibited the viability and function of SGC-7901 cells, except for the lowest dosages of AGPⅠ and AGPⅢ. There wa s a dose-effect relationship between the dosage of the AGP and SGC-7901 cells . The effect of the AGP at the molecular level was associated with the low prot ein expression of the c-myc and bcl-2 genes and the high protein expression of the p53, bax, fas and fas-L genes, as well as the cell factor TGFβ1. The i nhibitory effect of AGP was weaker than that of CDDP, but was stronger than that of Vitamine C. Conclusions Acanthopanax giraldii Harms Var. Hispidus Hoo polysaccharides selectively i nhibited the proliferation, the colony forming ability, and the viability and fu nction of human gastric cancer cells through the low protein expression of c-my c, bcl-2 and the high protein expression of p53, fas, fas-L and the cell facto r TGFβ1. The different inhibitory characteristics on the normal cells and c ancer cells are possibly caused by gene and the cell factor expressions.%目的研究红毛五加多糖对人胃癌细胞SGC-7901的诱导凋亡作用.方法采用细胞增殖法来研究时间-效应和剂量-效应.采用超微形态结构,凝胶电泳技术和流式细胞术(FCM)对细胞凋亡进行分析.结果 1.0×10-4mol/L AGP显著抑制了胃癌细胞的增殖. 胃癌细胞在1.0×10-4 m ol/L AGPⅣ作用36 h后,癌细胞浓缩、深染,胞膜起泡,致密的染色质沿核膜下凝聚,有凋亡小体形成;细胞DNA电泳呈现梯状带型;细胞周期分析G1峰前出现明显的细胞凋亡峰,定量分析凋亡细胞在1.0×10-4 mol/L AGPⅥ作用72小时发生率为62.6%.细胞周期分析表明四种红毛五加多糖均使细胞周期停滞在G0/G1期.结论 AGP对胃癌细胞的增殖抑制作用具有剂量-效应和时间-效应关系.AGP可诱导胃癌细胞凋亡 .AGPⅡ可能是AGPⅣ的主要有效成份.
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机译：目的探讨刺氨酸甘油的抑制作用危害伤害var。 Hispidus H OO多糖（AGP）对SGC-7901胃癌细胞及其可能的M机理。方法采用细胞倍增时间分析，采用菌落形成测定和MTT检测来研究抑制作用及其特征。我们还通过流式细胞术分析分析了由癌肠，抗肝癌和细胞因子表达的蛋白质的Amou NT.results AGP抑制了SGC-7901细胞和细胞群的增殖形成Abili Ty。 AGP在健康受试者和人胚胎鸟癣菌中没有抑制周边L血液的可活力和功能，除了AGP的高剂量（P <0.05），略微抑制两种类型正常的生存能力和功能细胞。 AGP抑制SGC-7901细胞的活力和功能，除了AGPⅠ和AGPⅢ的最低剂量外。 WA S在AGP和SGC-7901细胞的剂量之间的剂量效应关系。 AGP在分子水平下的效果与C-MYC和BCL-2基因的低PLAT EIN表达以及P53，BAX，FAS和FAS-L基因的高蛋白质表达以及细胞因子TGFβ1。 AGP的I烟型效果弱于CDDP，但比维生素C的效果较强。结论Acanthopanax Giraldii危害VAR。通过C-MY C，BCL-2和P53，FAS，Fas的高蛋白表达的低蛋白表达，选择性地扼杀了人胃癌细胞的增殖，菌落形成能力和人胃癌细胞的活力和Fu呈现-L和细胞事实上RTGFβ1。正常细胞和c uncer细胞上的不同抑制特性可能是由基因和细胞因子表达引起的。％不用于丛生的红腹加多糖对人胃癌细胞sgc-7901的诱导诱导作用。方法实用性。方法来 - 时间 - 效应和销量 - 效应。采采超微，凝胶电阻技术和流式细胞对对凋亡进行分享。结果1.0×10-4mol / l AGP显着抑制了胃癌细胞的增殖。胃癌细胞在1.0×10-4 m ol / lAGPⅳ作用36h后，癌细胞浓缩，深染，胞膜胞膜，致密的染色质核膜核膜，有凋亡小体形成;细胞dna电象呈现梯状带型;细胞细胞周析g1峰前出现明显的细胞凋亡峰，送量分凋亡在1.0×10-4 mol / lAGPⅵ作用2-4 mol / lAGPⅵ作用272％。细胞细胞阶段分享说明四种红毛五加多糖均使细胞细胞停滞停滞停滞停滞停滞停滞细胞细胞停滞结论结论胃癌细胞的增殖抑制作用具用品 - 效应和空间 - 效应agp可诱导胃癌凋亡凋亡.agpⅡ可怕是agp ange的成功。
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