共查询到19条相似文献，搜索用时 281 毫秒
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目的:探讨新城疫病毒(Newcastle disease virus,NDV)体外对S180肉瘤细胞(简称S180)生长有无抑制和诱导细胞凋亡作用。方法:取培养至对数生长期的S180细胞浓度为5×104/mL和1×106/mL分别接种于96孔板和50mL培养瓶中,加入不同浓度的NDV(1∶20、1∶10、1∶5)作用24h,分别用MTT法检测NDV对S180瘤细胞的生长抑制作用,荧光显微镜和琼脂糖凝胶电泳检测细胞凋亡。结果:经上述不同浓度的NDV作用24h,对S180细胞生长的抑制率依次为10%、26%、39%,各实验组吸光度值(A490)与对照组比较差异均有统计学意义(P<0.05)。荧光显微镜观察实验组培养的S180瘤细胞,出现细胞核固缩及凋亡小体,琼脂糖凝胶电泳见DNA梯形条带。结论:NDV对体外培养S180细胞增殖有明显抑制作用,可诱导S180细胞凋亡。 相似文献
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目的:研究地塞米松对胎鼠腭突中嵴上皮(Medial Edge Epithelium,MEE)细胞凋亡、增殖和分化的影响,以探讨地塞米松引起腭裂畸形的发病机制.方法:以醋酸地塞米松诱导胎鼠腭裂畸形,应用免疫组化法和图像分析研究MEE细胞中 bcl-2和p53基因在不同时期中实验组与对照组的表达情况.结果:实验组在GD13.5～16.5(GD,gestation day)MEE细胞的bcl-2 与p53表达总体维持增高趋势;GD13.5 MEE细胞的bcl-2 与p53表达实验组与对照组均无明显差别;GD14.5 MEE细胞的bcl-2与p5表达实验组明显多于对照组(P<0.01).结论:地塞米松诱发腭裂出现MEE细胞凋亡减少,通过改变MEE细胞中bcl-2和p53基因的表达而实现对MEE细胞增殖与凋亡的调控是地塞米松引起腭裂可能机制之一. 相似文献
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目的 :研究新城疫病毒在体外抗胃癌细胞活性及其与细胞凋亡的关系。方法 :应用倒置显微镜观察细胞形态、MTT法测NDV在体外对BGC - 82 3的抑制和杀伤作用 ,同时用流式细胞术检测胃癌细胞凋亡情况及细胞分裂周期各时象的变化。结果 :NDV在体外可使BGC - 82 3胃癌细胞形成明显的细胞病变效应、细胞生长抑制及细胞凋亡 ,且细胞凋亡率与感染时间呈正相关。G2、S期细胞减少 ,增殖指数 (PI)降低 ,与阴性对照组比较有显著性差异 (P<0 .0 1)。结论 :NDV具有显著的抗BGC - 82 3胃癌细胞活性。 相似文献
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目的:观察新型组蛋白去乙酰化酶( Histone Deacetylases,HDACs)抑制剂DWP0016对神经胶质瘤U251细胞株的作用,探讨诱导U251细胞周期阻滞及凋亡作用的机制.方法:采用噻唑蓝(MTT)法检测DWP0016对U251细胞株的增殖抑制作用;采用流式细胞术观察DWP0016对U251细胞周期的影响及凋亡诱导作用;采用实时定量PCR(real-time PCR)检测抑癌因子P21,P53的mRNA水平变化;蛋白免疫印迹法(Western blotting)测定Ac-H3,P21,P53,Pi3K,p-Pi3K,Akt,p-Akt的蛋白表达并进行光密度定量.结果:DWP0016抑制U251细胞增殖的半数抑制浓度(IC50=0.531 μmol·L-1)明显低于阳性对照奥沙利铂(IC50=4.792 μmol·L-1),组蛋白H3乙酰化水平显著上升;DWP0016作用后,U251细胞中细胞周期阻滞于G1期并产生凋亡,P21,P53的mRNA水平和蛋白水平明显上升,Pi3K/Akt通路中的Pi3K,Akt的磷酸化水平下降.结论:DWP0016能明显抑制U251细胞增殖,诱导细胞周期阻滞和凋亡产生,其机制与促进抑癌因子P21,P53的转录及蛋白表达,抑制细胞中Pi3K/Akt生长信号通路有关,具有良好的抗神经胶质瘤潜力和开发应用前景. 相似文献
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Bing-yu CHEN Lu-xi JIANG Ke HAO Lu WANG Ying WANG Yi-wei XIE Jian SHEN Meng-hua ZHU Xiang-ming TONG Kai-qiang LI Zhen WANG 《Journal of Zhejiang University. Science. B》2018,(6)
目的:评估血浆输注对脂多糖半乳糖诱导的小鼠急性肝损伤的保护作用,并探讨其作用机制。创新点:在小鼠急性肝损伤模型中证明血浆输注对肝损伤的保护作用,且此作用与p53介导的肝细胞凋亡相关。方法:将40只清洁型ICR雄性小鼠随机分为4组(n=10每组):(1)对照组;(2)血浆(plamsa)组。收集血清和肝组织样本,用天门冬氨酸转氨酶(AST)和丙氨酸氨基转移酶(ALT)试剂盒检测血清中AST和ALT水平;用酶联免疫吸附法(ELISA)检测肝组织中白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)的表达变化;肝组织进行苏木精-伊红染色法(HE)和网状纤维染色,显微镜下观察肝组织病理学变化;用免疫印迹法(WB)检测凋亡相关蛋白的变化。在腹腔注射后32小时内对小鼠进行存活分结论:能够显著诱导小鼠的急性肝损伤,包括增加血清中AST和ALT水平;中心小叶坏死和炎性细胞的组织病理学变化和炎症上(TNF-α和IL-6)。当血浆输注后,这些变化被缓解。结果显示,血浆输注显著降低小鼠死亡率,降低AST、ALT和炎症因子如TNF-α和IL-6的水平。Cleaved Caspase-3、BAX和p53的表达下调,Bcl-2上调,表明血浆可以减少诱导的细胞凋亡。血浆输注对诱导的急性肝损伤的保护机制与通过p53诱导的凋亡途径和炎症因子减少相关。 相似文献
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目的:通过比较阿霉素(ADR)作用的视网膜色素上皮细胞(ARPE-19)和正常ARPE-19间的差异表达基因和信号通路,探究ADR治疗玻璃体视网膜增殖性疾病的潜在机制。创新点:首次运用基因芯片技术通过比较转录组学分析探究ADR促进ARPE-19细胞凋亡的机制。方法:采用磺酰罗丹明B(sulforhodamine B,SRB)比色法和碘化丙啶(PI)单染结合流式细胞术检测ADR对ARPE-19细胞的增殖抑制作用;通过基因芯片技术筛选ADR作用的ARPE-19细胞(实验组)和正常ARPE-19细胞(对照组)间的差异表达基因和相关信号通路;用JC-1染色结合流式细胞术和Bcl2/Bax蛋白表达比率检测线粒体功能;通过检测γ-H2AX、p-CHK1、 p-CHK2等蛋白表达量分析DNA的损伤和修复。结论:ADR通过启动DNA损伤反应,引起p53信号通路依赖的线粒体功能失调并激活caspase依赖的凋亡,最终导致ARPE-19细胞死亡。 相似文献
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目的:为了探讨细胞凋亡促进基因bax在尿路上皮癌中染色的表达及意义以及与p53蛋白表达的相互关系。方法:对65例尿路上皮癌石蜡标本进行免疫组化。结果:bax蛋白阳性率为50.77％,且与肿瘤病理分级有关,其阳性细胞主要分布于高分化癌及浅表性癌。分级间比较有显著性差异(P<0.05)。分期间比较差异无显著性。p53蛋白阳性率为46.15％,与bax相反,在低分化及浸润性癌组织阳性率明显高于高分化及浅表性癌(P<0.05)。结论:作为细胞凋亡促进基因bax丢失与p53基因突变一样与尿路上皮癌的发生发展有关。检测bax与D53基因蛋白可进一步了解尿路上皮癌生物学信息,也为临床提供更有价值的预后判断指标。 相似文献
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目的：研究鹅绒委陵菜多糖（PAP）的抗肿瘤作用及其免疫调节作用。方法：用小鼠肝癌（S180）移植肿瘤的动物模型,以肿瘤抑制率、溶血素、NK细胞活性和淋巴细胞增殖率作指标,结果表明,鹅绒委陵菜多糖不仅能显著抑制移植性肿瘤S180的生长,而且还能明显促进荷瘤鼠的体液免疫和提高荷瘤鼠的脾细胞转化功能及增强NK细胞活性,均以200mg。kg-1.d-1效果最佳。结论：鹅绒委陵菜多糖的抗肿瘤作用和其免疫调节作用有明显的相关性,鹅绒委陵菜多糖的抗肿瘤作用可能与激活体内免疫系统有关。 相似文献
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目的:原核表达并纯化大型溞胆碱酯酶(ChE),制备鼠抗大型溞ChE多克隆抗体,并对抗体的适用性进行研究。创新点:首次通过原核表达获得了大型溞重组ChE蛋白,通过免疫小鼠获得了高效价、高特异性的多克隆抗体,通过样品检测证明了抗体的适用性。方法:利用聚合酶链式反应(PCR)技术获得大型溞ChE基因编码序列,并将其亚克隆至原核表达载体p ET-29a(+),构建重组表达质粒p ET-ChE,用异丙基硫代半乳糖苷(IPTG)诱导重组蛋白的表达;对表达产物进行聚丙烯酰胺凝胶电泳(SDS-PAGE)和酶活性检测,并对蛋白进行纯化(图4);使用纯化蛋白免疫BALB/c小鼠,制备多克隆抗体(图5),用酶联免疫吸附分析法(ELISA)对处于三唑磷和低温胁迫下以及经反复冻融处理的大型溞体内的ChE含量变化进行检测(图7、表6和7),以评价抗体的可适用性。结论:获得了高纯度的ChE重组蛋白;免疫小鼠后,获得了特异性强、高效价的抗体;通过对处于三唑磷和低温胁迫下以及经过反复冻融处理的大型溞体内的ChE含量的检测,证明了抗体的适用性。 相似文献
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<正>1原题呈现例题中外科学家经多年合作研究,发现circDNMT1 (一种RNA分子)通过与抑癌基因p53表达的蛋白结合诱发乳腺癌,为解决乳腺癌这一威胁全球女性健康的重大问题提供了新思路。下列叙述错误的是(C)A. p53基因突变可能引起细胞癌变B.p53蛋白能够调控细胞的生长和增殖C.circDNMT1高表达会使乳腺癌细胞增殖变慢D.circDNMT1的基因编辑可用于乳腺癌的基础研究 相似文献
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The growth inhibitory effects of D-glucosamine hydrochloride （GlcNH2-HCl）, D-glucosamine （GlcNH2） and N-acetyl glucosamine （NAG） on human hepatoma SMMC-7721 cells in vitro were investigated. The results showed that GlcNH2.HCl and GlcNH2 resulted in a concentration-dependent reduction in hepatoma cell growth as measured by MTT （3-（4,5-dimethylthiazol- 2-yl）-2,5-diphenyltetrazolium bromide） assay. This effect was accompanied by a marked increase in the proportion of S cells as analyzed by flow cytometry. In addition, human hepatoma SMMC-7721 cells treated with GlcNH2-HCl resulted in the induction of apoptosis as assayed qualitatively by agarose gel electrophoresis. NAG could not inhibit the proliferation of SMMC-7721 cells. GlcNH2-HCl exhibited antitumor activity against Sarcoma 180 in Kunming mice at dosage of 125-500 mg/kg, dose of 250 mg/kg being the best. GlcNH2-HCl at dose of 250 mg/kg could enhance significantly the thymus index, and spleen index and could promote T lymphocyte proliferation induced by ConA. The antitumor effect of GlcNH2-HCl is probably host-mediated and cytocidal. 相似文献
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盐生隐杆藻胞外多糖(EPAH)抗肿瘤作用的实验研究 总被引：1，自引：0，他引：1
目的:探讨盐生隐杆藻胞外多糖对小鼠抗肿瘤作用的影响.方法:建立小鼠移植性S180实体瘤模型,观察EPAH对S180荷瘤小鼠的抑瘤作用、对白细胞的数量、对免疫器官及红细胞粘附肿瘤细胞能力的影响;另建立小鼠移植性S180腹水瘤模型,观察EPAH对小鼠存活时间的影响;同时,通过体外培养检测EPAH对SMMC7721细胞增殖的影响.结果:EPAH能明显抑制S180、SMMC7721细胞生长、促进红细胞粘附肿瘤细胞能力、增强免疫力并能有效提升减少的白细胞数量.结论:EPAH能显著增强小鼠抗肿瘤活性. 相似文献
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Shao-xiang Weng Mei-hua Sui Shan Chen Jian-an Wang Geng Xu Ji Ma Jiang Shan Lu Fang 《Journal of Zhejiang University. Science. B》2009,10(7):528-535
Objective This study is to determine the effect of the natural product parthenolide, a sesquiterpene lactone isolated from extracts
of the herb Tanacetum parthenium, on the proliferation of vascular smooth muscle cells (VSMCs).
Methods Rat aortic VSMCs were isolated and cultured in vitro, and treated with different concentrations of parthenolide (10, 20 and
30 μmol/L). [3H]thymidine incorporation was used as an index of cell proliferation. Cell cycle progression and distribution were determined
by flow cytometric analysis. Furthermore, the expression of several regulatory proteins relevant to VSMC proliferation including
IκBα, cyclooxygenase-2 (Cox-2), p21, and p27 was examined to investigate the potential molecular mechanism.
Results Treatment with parthenolide significantly decreased the [3H]thymidine incorporation into DNA by 30%∼56% relative to control values in a dose-dependent manner (P<0.05). Addition of parthenolide also increased cell population at G0/G1 phase by 19.2%∼65.7% (P<0.05) and decreased cell population at S phase by 50.7%∼84.8% (P<0.05), which is consistent with its stimulatory effects on p21 and p27. In addition, parthenolide also increased IκBα expression
and reduced Cox-2 expression in a time-dependent manner.
Conclusion Our results show that parthenolide significantly inhibits the VSMC proliferation by inducing G0/G1 cell cycle arrest. IκBα and Cox-2 are likely involved in such inhibitory effect of parthenolide on VSMC proliferation. These
findings warrant further investigation on potential therapeutic implications of parthenolide on VSMC proliferation in vivo.
Project (No. 491020-W50315) supported by the Foundation of the Health Bureau of Zhejiang, China 相似文献
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目的：研究峨眉岩白菜提取物体内外抗肝肿瘤作用。方法：应用MTT法和移植性S180实体荷瘤小鼠。研究不同剂量提取物的体内体外抗肿瘤作用。结果：峨眉岩白菜提取物对体外培养的人肺癌A549细胞增殖有显著的抑制作用。抑制作用与浓度有明显的依赖关系,且随提取浓度的增大,抑制效果越好;荷瘤小鼠模型研究表明,提取物对S180有显著的抑制作用,当剂量为400mg/kg时对肿瘤的抑制效果最好,抑瘤率达52.11％。 相似文献
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Xu Q Li ZX Peng HQ Sun ZW Cheng RL Ye ZM Li WX 《Journal of Zhejiang University. Science. B》2011,12(4):247-255
This paper aims to investigate the effects of artesunate (ART) on growth and apoptosis in human osteosarcoma HOS cell line
in vitro and in vivo and to explore the possible underlying mechanisms. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium
bromide (MTT) assay. The induction of apoptosis was detected by light and transmission electron microscopy and flow cytometry.
Western blot analysis was used to investigate the related mechanisms. Nude mice were further employed to investigate the antitumour
activity of ART in vivo. MTT assay results demonstrated that ART selectively inhibits the growth of HOS cells in a dose- and
time-dependent manner. Based on the findings of light and transmission electron microscopy, Hoechst 33258 staining, and fluorescein
isothiocyanate (FITC)-annexin V staining, the cytotoxicity of ART in HOS cells occurs through apoptosis. With ART treatment,
cytosolic cytochrome c was increased, Bax expression was gradually upregulated, Bcl-2 expression was downregulated, and caspase-9 and caspase-3
were activated. Thus, the intrinsic apoptotic pathway may be involved in ART-induced apoptosis. Cell cycle analysis by flow
cytometry indicated that ART may induce cell cycle arrest at G2/M phase. In nude mice bearing HOS xenograft tumours, ART inhibited tumour growth and regulated the expressions of cleaved
caspase-3 and survivin, in agreement with in vitro observations. ART has a selective antitumour activity against human osteosarcoma
HOS cells, which may be related to its effects on induction of apoptosis via the intrinsic pathway. The results suggest that
ART is a promising candidate for the treatment of osteosarcoma. 相似文献
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Fang YANG Wang-wang LIU Hui CHEN Jia ZHU Ai-hua HUANG Fei ZHOU Yi GAN Yan-hua ZHANG Li MA 《Journal of Zhejiang University. Science. B》2020,21(1):64-76
目的:最近有研究表明卡非佐米(Carfilzominb,CFZ)能有效抑制肺腺癌细胞生长,但是其中的内在机制仍然需要进一步研究。本文针对CFZ抑制肺腺癌生长机制进行了系统研究。创新点:揭示了蛋白酶体抑制剂抗实体肿瘤的新机制,为这类药物用于实体肿瘤治疗提供了有利依据。同时Gadd45a可做为候选指标用于蛋白酶体抑制剂抗肿瘤疗效的预测。方法:应用流式细胞术检测CFZ对肺腺癌细胞周期和凋亡的影响;通过MTS比色法及平板克隆形成实验分析CFZ对肺腺癌细胞生长的抑制作用;使用蛋白质印迹法(western blot)和定量聚合酶链反应(qPCR)检测相关基因表达水平的改变。结论:CFZ通过AKT/FOXO3a通路上调Gadd45a基因的表达,诱导肺腺癌细胞周期阻滞和凋亡,从而发挥抗肿瘤效应。 相似文献
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Ning SONG Yan WANG Xiao-dong GU Zong-you CHEN Liu-bin SHI 《Journal of Zhejiang University. Science. B》2013,14(6):451-459
Eukaryotic initiation factor subunit c(eIF3c) has been identified as an oncogene that is over-expressed in tumor cells and,therefore,is a potential therapeutic target for gene-based cancer treatment.This study was focused on investigating the effect of small interfering RNA(siRNA)-mediated eIF3c gene knockdown on colon cancer cell survival.The eIF3c gene was observed to be highly expressed in colon cancer cell models.The expression levels of the gene in eIF3c siRNA infected and control siRNA infected cells were compared via real-time polymerase chain reaction(PCR) and western blotting analysis.Cell proliferation levels were analyzed employing 3-(4,5-dimethylthiazol 2-yl)-2,5-diphenyltetrazolium bromide(MTT) and colony formation assays.Furthermore,the effects of eIF3c gene knockdown on the cell cycle and apoptosis were analyzed using flow cytometry.The results showed that suppression of eIF3c expression significantly(P<0.001) reduced cell proliferation and colony formation of RKO colon cancer cells.The cell cycle was arrested by decreasing the number of cells entering S phase.Further,apoptosis was induced as a result of eIF3c knockdown.Collectively,eIF3c deletion effectively reduced the survival of colon cancer cells and could be used as a therapeutic tool for colon cancer therapy. 相似文献