陌上菜提取物对A549肺癌小鼠移植瘤影响的实验研究

目的:探讨陌上菜(BSC)提取物对A549肺癌小鼠移植瘤的影响。方法:建立A549肺癌小鼠移植瘤模型,观察BSC对A549肺癌小鼠移植性肿瘤的体积、瘤重、抑瘤率、体重的影响。结果:BSC对A549肺癌的生长有明显抑制作用,抑瘤率大于40%;与阴性组比较,对A549肺癌BALB/c-nu小鼠体重无任何影响。结论:BSC可抑制A549肺癌的生长。     

肺癌A549耐药裸鼠移植瘤模型的建立

目的探讨肺癌A549耐药裸鼠移植瘤模型的建立方法,为克服肿瘤多药耐药新药的筛选提供体内研究的模型。为进行肿瘤的体内相关研究和抗癌药物的筛选提供实验基础。方法使用顺铂诱导肺癌A549细胞,以建立其多药耐药细胞株A549/DDP;MTT细胞毒实验检测细胞对顺铂的敏感性;皮下接种法建立裸鼠移植瘤模型;绘制移植瘤生长曲线,观察其增值特性。结果经过8个月的诱导建立了肺癌顺铂耐药细胞株A549/DDP;MTT细胞毒实验结果显示与A549细胞比较,A549/DDP细胞对顺铂约耐药8倍,并且A549/DDP耐药细胞建立的裸鼠移植瘤仍然保持对顺铂的耐药性;生长曲线结果显示A549/DDP细胞裸鼠移植瘤的增殖速度与A549细胞之间没有显著性差异。结论成功建立了肺癌A549/DDP耐药细胞裸鼠移植瘤模型,可为肺癌耐药的研究提供较理想的动物模型。     

消积饮对人A549肺癌细胞增殖的抑制作用

目的观察消积饮对人肺癌细胞株A549细胞增殖的影响。方法选取人A549肺癌细胞株作为研究对象,生长于RPMI 1640培养液中,细胞传代24 h进入对数生长期后分别加入低、中、高剂量含药血清(灌胃给予消积饮后的大鼠血清)及对照组大鼠血清进行细胞诱导。MTS法测定消积饮对A549细胞增殖的抑制作用。结果不同剂量的消积饮血清均可抑制人A549肺癌细胞的增殖,抑制率明显高于对照组(P<0.01)。消积饮高、中剂量组抑制率明显高于低剂量组(P<0.05),但高剂量组与中剂量组之间无明显差异。结论消积饮可在体外有效抑制人肺癌细胞株A549细胞的生长,在一定浓度范围内,具有量效关系。     

枸杞多糖对人肺癌A549细胞影响的研究

目的:探讨枸杞多糖(LBP)对人肺癌A549细胞的影响及作用机制。方法:将LBP作用于肺癌A549细胞,应用M TT法、电镜和钙离子测定等技术测定LBP的抗肿瘤作用及作用机理。结果:LBP呈剂量依赖性(100m g/L~2000m g/L)地抑制人肺癌A549细胞的增殖,诱导其凋亡,并可使细胞内钙离子浓度升高。结论:LBP可诱导A549细胞凋亡,其作用机制可能与细胞内钙离子浓度升高有关。     

雷公藤红素对人肺癌A549细胞增殖活性及能量代谢的影响

目的 探究雷公藤红素对人肺癌细胞（A549）的增殖活性以及能量代谢的影响。方法 噻唑蓝(MTT)法和生长曲线检测雷公藤红素对细胞的增殖抑制情况;HE染色观察细胞形态变化;分光光度法测定糖酵解途径中己糖激酶（HK）、丙酮酸激酶（PK）、乳酸脱氢酶（LDH）活力和三羧酸循环中琥珀酸脱氢酶（SDH）活力及能量代谢终产物ATP的含量。结果 雷公藤红素对A549细胞有增殖抑制作用,浓度在2 μg?mL^-1时,对A549细胞的抑制率达到62.71%,远远大于阳性药组5-FU的抑制率;生长曲线结果显示,雷公藤红素作用第4天细胞浓度最低,第6天细胞抑制程度最明显;HE结果表明雷公藤红素处理48 h后,细胞形态变圆,体积缩小,核深染且颜色变深;试剂盒检测结果显示,雷公藤红素非常显著的降低乳酸脱氢酶酶活力（P<0.01）,显著降低琥珀酸脱氢酶活力和ATP含量均显著降低(P<0.05),但对己糖激酶和丙酮酸激酶无明显作用。结论 雷公藤红素能够显著降低人肺癌A549细胞中乳酸脱氢酶和琥珀酸脱氢酶的活力,干扰能量代谢,抑制能量ATP生成,达到抑制A549细胞增殖的作用。     

岩龙胶囊对Lewis肺癌小鼠的抑瘤作用研究

目的探究岩龙胶囊对Lewis肺癌瘤株转染的C57BL/6小鼠的抑瘤作用,为临床提供理论依据。方法将50只成功Lewis肺癌瘤株转染的C57BL/6小鼠随机分为5组:岩龙胶囊高(A)、中(B)、低剂量(C)组,阳性对照(D)组,阴性对照(E)组,每组10只。造模后第8天,A、B、C组灌胃给中药,每天一次;D组每天腹腔注射顺铂注射液(DDP)一次,四组共给药7天。E组每天用等体积生理盐水灌胃共7天。继后继续观察7天,记录小鼠一般情况,实验结束后处死小鼠检测各项指标。结果①岩龙胶囊组均能降低瘤重指数,与E组对比,A、C组P值均<0.001,B组P<0.01,均有统计学意义;②A、C组能减少肺癌小鼠的肺转移结节数,与E组对比P<0.05,有统计学意义。结论岩龙胶囊能够降低Lewis肺癌荷瘤小鼠的瘤重指数,有一定的抑制肿瘤作用;能够减少肺转移结节数,有一定的抑制肿瘤转移作用。     

黄芪多糖对人肺癌A549 细胞增殖的作用及其机制的实验研究

目的探讨黄芪多糖（astragalus polysaccharide,APS）对人肺癌A549细胞增殖的作用及其机制。方法用不同浓度的APS（25μg.mL-1、50μg.mL-1、10μg.mL-1、200μg.mL-1、400μg.mL-1）作用于人肺癌A549细胞,用MTT法检测细胞增殖的抑制率,免疫细胞化学法检测bcl-2和bax的表达。结果 APS的浓度在25μg.mL-1～400μg.mL-1范围内均可抑制人肺癌A549细胞的增殖,100μg.mL-1的APS对A549细胞增殖的抑制率达最高,100μg.mL-1的APS作用于人肺癌A549细胞48和72小时后,均可下调bcl-2和上调bax的表达。结论 APS能够可抑制人肺癌A549细胞的增殖,可能与其下调bcl-2和上调bax的表达有关。     

TNF-α对人肺癌A549细胞凋亡的影响

目的探讨TNF-α对人肺癌A549细胞凋亡的影响;方法培养人肺癌A549细胞,与TNF-α(10、100U·ml-1)共孵育,通过Western blot分析P53蛋白表达的变化,同时利用Annexin V/PI双染色流式细胞仪,检测人肺癌A549细胞凋亡率的变化。结果与空白组相比,TNF-α组的P53蛋白表达明显升高,且细胞凋亡率也明显升高,分别为1.22±0.62和1.65±0.38(P<0.01)。结论TNF-α可以诱导人肺癌A549细胞凋亡,从而可能起到抗肿瘤的疗效。     

SDZ诱导肺癌A549细胞凋亡

目的旨在探讨SDZ体外对肺癌A549细胞生长的作用。方法采用hoechst染色、荧光显微镜下观察SDZ诱导肺癌A549细胞凋亡的作用。结果经SDZ1000μg／ml作用24h肿瘤细胞即可发生凋亡,凋亡率达31．7％。结论SDZ体外可诱导肺癌A549细胞凋亡。     

miR-214对人肺癌A549细胞增殖和侵袭能力的影响

目的:通过构建miR-214的真核表达载体,研究其对人肺癌A549细胞增殖和侵袭能力的影响。方法:以A549细胞基因组DNA为模板,扩增得到miR-214前体序列,插入表达载体pcDNA3.1(+)克隆获得pcDNA3.1(+)-miR-214。将真核表达载体pcDNA3.1(+)-miR-214转染到A549细胞中,并采用实时荧光定量PCR(real-time PCR)对其表达情况进行验证。采用MTT和transwell小室等方法分别检测转染重组质粒pcDNA3.1(+)-miR-214对A549细胞增殖能力和侵袭能力的影响。结果:成功构建了miR-214稳定过表达的真核表达载体pcDNA3.1(+)-miR-214;real-time PCR检测结果表明,转染pcDNA3.1(+)-miR-214后A549细胞中miR-214过表达(P<0.05)。miR-214过表达后A549细胞的增殖和侵袭能力均明显降低。结论:miR-214在A549细胞中过表达能够抑制细胞的增殖和侵袭能力,为进一步深入研究miR-214在肿瘤中的作用机制提供了实验依据。     

Antitumor activity of ascorbic acid in combination with antitumor agents against Lewis lung carcinoma

Antitumor activity of ascorbic acid in combination with antitumor agents (mitomycin C and 5-fluorouracil) was examined against subcutaneously implanted Lewis lung carcinoma-bearing C57BL/6 mice by feeding them an ascorbic acid-deficient diet. The mice were divided into four groups: group 1 received intraperitoneally mitomycin C (2 mg/kg) and 5-fluorouracil (50 mg/kg) once a week for four weeks beginning from the day after implantation of tumors, as well as ascorbic acid (1000 mg/kg) twice a week for the same four weeks; group 2 received only mitomycin C and 5-fluorouracil; group 3 received only ascorbic acid; group 4 received a vehicle (physiological saline). Tumor growth of group 1 compared with the other three groups, and that of group 2 compared with groups 3 and 4, was significantly inhibited by day 13 post implantation. Histological examinations of tumor tissues at 10 days after implantation of tumors already showed degenerative changes which indicated these antitumor effects.     

康莱特注射液在Lewis肺癌中对肿瘤生长及EGFR蛋白表达的影响

目的：探讨康莱特注射液（KLT）对小鼠Lewis肺癌生长及对表皮生长因子受体（EGFR）蛋白表达的影响。方法：建立小鼠Lewis肺癌模型,将40只接种Lewis肺癌细胞的C57BL/6小鼠随机分成4组：模型对照组、KLT低剂量组（6.25mL/kg）、KLT中剂量组（12.5mL/kg）、KLT高剂量组（25mL/kg）,每组10只。小鼠连续腹腔注射KLT注射液14d,于接种后第16天处死小鼠,测量瘤重及体重,计算肿瘤抑制率,提取肿瘤组织总蛋白,通过Westernblot法检测肿瘤组织EGFR的蛋白表达情况。结果：KLT注射液能明显抑制Lewis肺癌小鼠肿瘤的生长,影响肿瘤组织的形态及组织学改变,并能降低肿瘤组织中EGFR的蛋白表达量。结论：KLT注射液可明显抑制小鼠Lewis肺癌的生长,其机制可能与抑制EGFR的蛋白表达有关。     

Antitumor activity of calcium in combination with antitumor agents against Lewis lung carcinoma

The antitumor activity of calcium gluconate in combination with mitomycin C and 5-fluorouracil was examined against subcutaneously implanted Lewis lung carcinoma-bearing C57BL/6 mice. The mice were divided into four groups: group 1 received mitomycin C (2 mg/kg) and 5-fluorouracil (50 mg/kg) intraperitoneally once a week for four weeks beginning from the day after implantation of tumors, as well as calcium gluconate (155 mg/kg) twice a week for the same four weeks; group 2 received only mitomycin C and 5-fluorouracil; group 3 received only calcium gluconate; group 4 received a vehicle (physiological saline). Significantly enhanced inhibition of tumor growth was observed neither in a comparison between groups 3 and 4, nor in a comparison between groups 1 and 2 (expect on day 20 post implantation). Thus calcium gluconate given alone or in combination with antitumor agents hardly appeared to possess effective antitumor activity.     

In vivo antitumor effect of endostatin-loaded chitosan nanoparticles combined with paclitaxel on Lewis lung carcinoma

The purpose of this study was to prepare endostatin-loaded chitosan nanoparticles (ES-NPs) and evaluate their antitumor effect when combined with paclitaxel (PTX) on Lewis lung carcinoma (LLC) mouse xenografts. ES-NPs were prepared by ionic cross-linking. Characterization of the ES-NPs included size distribution, drug-loading efficiency (DL), and encapsulation efficiency (EE). An in vitro release test was also used to determine the release behavior of the ES-NPs. A subcutaneous LC xenograft model of C57BL/6J mice was established. The mice were randomly divided into six groups: control (0.9% NaCl), ES, PTX, ES-NPs, ES?+?PTX, and ES-NPs?+?PTX. The tumor volume was dynamically measured for the duration of the experiment. Immunohistochemistry was performed to determine the Ki-67 and microvascular density (MVD) in each group. Serum vascular endothelial growth factor (VEGF) and ES levels were determined by enzyme-linked immunosorbent assay (ELISA). ES-NPs were successfully synthesized and had suitable size distribution and high EE. The NPs were homogenously spherical and exhibited an ideal release profile in vitro. In vivo, tumor growth was significantly inhibited in the ES-NPs?+?PTX group. The tumor inhibitory rate was significantly higher in the ES-NPs?+?PTX group than in the other groups (p?相似文献   

川芎嗪对小鼠Lewis肺癌的治疗作用

目的:研究中药川芎嗪(TMP)对实体肿瘤的疗效及其可能的作用机理。方法:本研究运用Lewis肺癌小鼠模型,观察TMP对小鼠Lewis肺癌的疗效、免疫功能、生存质量及不良反应的影响。结果:TMP治疗小鼠Lewis肺癌能抑制肿瘤的生长,稳定病灶,提高荷瘤小鼠的生存质量,改善免疫功能。结论:TMP对小鼠Lewis肺癌有明显疗效,其作用机理与其本身对Lewis肺癌实体瘤有抑制作用和提高荷瘤小鼠免疫功能有关。     

Augmented antitumor effects of erlotinib and cabozantinib on A549 non-small cell lung cancer: In vitro and in vivo studies

Non-small cell lung carcinoma is a challenging disease worldwide. This study aims to determine whether combining erlotinib, an epidermal growth factor receptor (EGFR) inhibitor, with cabozantinib, a mesenchymal-epithelial transition factor (c-Met) inhibitor, would have an augmented therapeutic benefit on A549 cells. The combination of erlotinib and cabozantinib (5 µM) inhibited A549 cell viability compared to each monotherapy at ≥ 10 µM as confirmed by the MTT assay. Combination therapy also has a more potent inhibition of cellular migration than monotherapy using the wound-healing assay. Furthermore, mRNA expression analyses for assessing apoptosis, metastasis, and cell cycle-related genes, the results showed that combination therapy significantly inhibits levels of BCL-2, MMP-9, VEGF, and TGF-β while inducing p53, p21, and BAX expression. In terms of oncogenic markers, western blotting analysis showed a significant reduction of BCl-2 expression and elevation in caspase3, p53, and p21 proteins as indicators of cell death via apoptosis. The antitumor in vivo effect of the combination therapy showed significant tumor inhibition compared to monotherapy. In conclusion, combination therapy could be a potential promising strategy to treat non-small cell lung carcinoma.     

Involvement of doxorubicin-induced Fas expression in the antitumor effect of doxorubicin on Lewis lung carcinoma in vivo

Deficiency of Fas expression is one of mechanisms involved in the immune evasion by tumors. Several antitumor drugs, such as doxorubicin (DOX) increase Fas expression in tumor cells and sensitize the cells to Fas-mediated apoptosis in vitro. However, the significance of the Fas expression in vivo is still unclear. Therefore, we examined a role of Fas expression on antitumor effect of DOX using a syngeneic tumor model of Lewis lung carcinoma (3LL) cells in C57BL/6-gld mice that lack functional Fas ligand (FasL). In vitro, anti-Fas agonistic antibody, Jo2, did not decrease a viable cell number of 3LL cells in the absence of DOX, whereas it significantly reduced the cell viability in the presence of DOX. The treatment with DOX alone at the same dose did not induce cell death. Flowcytometric analysis of Fas expression revealed that 3LL cells expressed only a marginal amount of Fas, but the treatment of the cells with DOX increased the expression of Fas in the cell surface. When splenic T cells were prepared from 3LL-bearing C57BL/6 mice, the splenic T cells significantly killed DOX-pretreated 3LL cells more than untreated 3LL cells. In the syngeneic models, DOX inhibited growth of 3LL solid tumor both in wild-type C57BL/6 mice and in Fas-deficient C57BL/6-lpr mice, but it failed in C57BL/6-gld mice, suggesting that the interaction between host FasL and tumor Fas is involved in the antitumor effect of DOX. Furthermore, Fas expression was increased in the solid tumor by the treatment of DOX. These results suggest that the antitumor effect of DOX is partly exerted by the Fas expression and host immune defense.     

Ad-ING4抑制人A549肺癌细胞及其裸鼠移植瘤的生长

目的 研究腺病毒介导的ING4基因(Ad-ING4)对肺癌体内外的抑制作用及其潜在的分子机制.方法 体外采用50 MOI的Ad-ING4感染A549肺癌细胞,并用MTT法检测Ad-ING4对A549细胞的抑制作用,流式细胞仪检测肿瘤细胞的凋亡率.采用A549细胞株建立人肺癌裸鼠模型,瘤体局部注射干预用药,每隔5天测量一次肿瘤体积,并计算瘤重抑瘤率;瘤块免疫组化检测ING4、生存素(survivin)、CD34、HIF-1等基因的表达.结果 Ad-ING4感染A549细胞抑制率可达47.62%;72 h凋亡率为18.5%;荷瘤裸鼠经治疗后,Ad-ING4组和顺铂(DDP)组的肿瘤体积、瘤重均明显缩小,其抑瘤率分别达到42.43%和46.47%,DDP组出现不良反应;免疫组化检测Ad-ING4组和DDP组与对照组比较,生存素、CD34、HIF-1的表达下调(P<0.01).结论 Ad-ING4对人A549肺癌细胞及其裸鼠移植瘤的生长具有明显的抑制作用.其抑瘤机制可能与下调生存素、CD34、HIF-1的基因表达进而诱导肿瘤细胞凋亡和抑制肿瘤血管形成等有关.     

Comparison of the effects of auranofin and retinoic acid on plasminogen activator activity of peritoneal macrophages and Lewis lung carcinoma cells

Urokinase-type plasminogen activator, a neutral proteinase, seems to play a central role in the degradation of the extracellular matrix that accompanies a number of biological phenomena including inflammatory reactions and neoplasia. The effect of auranofin and retinoic acid on the plasminogen activator activity expressed by two cell types, i.e. murine macrophages and Lewis lung carcinoma cells, has been investigated. Low concentrations of both drugs (10(-6)-10(-7) M) can inhibit in vitro the induction of plasminogen activator in macrophages stimulated by phorbol 12-myristate 13-acetate. This action occurs rapidly (15 min), is irreversible and is independent of a global cytotoxic effect. Auranofin and retinoic acid remain without effect in macrophages when added after stimulation by the phorbol ester. Both drugs are thus potent inhibitors of the induction of plasminogen activator activity in macrophages, possibly through an interaction with the protein kinase C system. The plasminogen activator activity of Lewis lung carcinoma cells, which is apparently not dependent on a protein kinase C pathway, is not influenced by auranofin or retinoic acid. These observations may contribute to explain: (1) the activity of auranofin and retinoic acid in rheumatoid arthritis, and (2) the antitumor promoting activity of retinoic acid. It would be relevant to assess whether auranofin may exhibit, like retinoic acid, an antitumor-promoting activity.     

绿原酸抗小鼠CT26结肠癌作用的研究

目的考察绿原酸对小鼠CT26结肠癌移植瘤生长的抑制作用。方法以荷瘤小鼠实体瘤重、抑瘤率及对脾脏、胸腺指数的影响为指标,并结合肿瘤细胞的病理切片,评价绿原酸对CT26结肠癌的抑制作用。结果与阴性组比较,从抑瘤率及组织病理切片,可知绿原酸对CT26结肠癌移植瘤有明显的抑制作用。结论绿原酸具有一定的抗CT26结肠癌作用。