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1.

BACKGROUND/OBJECTIVES

D. candidum is a traditional Chinese food or medicine widely used in Asia. There has been little research into the anticancer effects of D. candidum, particularly the effects in colon cancer cells. The aim of this study was to investigate the anticancer effects of D. candidum in vitro and in vivo.

MATERIALS/METHODS

The in vitro anti-cancer effects on HCT-116 colon cancer cells and in vivo anti-metastatic effects of DCME (Dendrobium canidum methanolic extract) were examined using the experimental methods of MTT assay, DAPI staining, flow cytometry analysis, RT-PCR, and Western blot analysis.

RESULTS

At a concentration of 1.0 mg/mL, DCME inhibited the growth of HCT-116 cells by 84%, which was higher than at concentrations of 0.5 and 0.25 mg/mL. Chromatin condensation and formation of apoptotic bodies were observed in cancer cells cultured with DCME as well. In addition, DCME induced significant apoptosis in cancer cells by upregulation of Bax, caspase 9, and caspase 3, and downregulation of Bcl-2. Expression of genes commonly associated with inflammation, NF-κB, iNOS, and COX-2, was significantly downregulated by DCME. DCME also exerted an anti-metastasis effect on cancer cells as demonstrated by decreased expression of MMP genes and increased expression of TIMPs, which was confirmed by the inhibition of induced tumor metastasis in colon 26-M3.1 cells in BALB/c mice.

CONCLUSIONS

Our results demonstrated that D. candidum had a potent in vitro anti-cancer effect, induced apoptosis, exhibited anti-inflammatory activities, and exerted in vivo anti-metastatic effects.  相似文献   
2.
目的:探讨榄香烯对人胃癌细胞株SGC-7901体外生长及细胞黏附分子CD44v6、CD44的影响。方法:Cell Counting Kit-8(CCK-8)检测榄香烯对SGC-7901细胞增殖的影响;采用DAPI荧光染色法进行细胞核形态学分析;流式细胞仪检测细胞膜表面CD44v6、CD44表达。结果:榄香烯抑制SGC–7901细胞增殖,其呈量效和时效关系;DAPI染色显示榄香烯诱导SGC-7901细胞凋亡并显示特征性的凋亡细胞核形态;流式细胞仪检测结果显示榄香烯20、30、40μg/mL组与对照组相比,SGC-7901细胞膜表面CD44v6表达明显减少(P〈0.01),CD44表达的差异无统计学意义(P〉0.05)。结论:榄香烯能抑制SGC-7901细胞增殖、诱导细胞凋亡,其抗肿瘤转移的机制可能与下调CD44v6表达相关。  相似文献   
3.
利用多种色谱分离方法和波谱学鉴定方法对宽叶金粟兰乙酸乙酯部位的化学成分进行了分离鉴定,并借助药理学方法对其中得到的部分化合物进行了抗乳腺癌转移活性的初步筛选。总共从宽叶金粟兰乙酸乙酯部位中分离得到15个倍半萜及其二聚体类化合物,分别鉴定为zedoarofuran(1),chlorajapolide D(2),4β,8β-dihydroxy-5α(H)-eudesm-7(11)-en-8,12-olide(3),curcolonol(4),lasianthuslactone A(5),chlomultin C(6),(1E,4Z)-8-hydroxy-6-oxogermacra-1(10),4,7(11)-trieno-12,8-lactone(7),shizukanolide E(8),shizukanolide F(9),9α-hydroxycurcolonol(10),shizukaol B(11),shizukaol C(12),cycloshizukaol A(13),sarcandrolide B(14),henriol A(15)。其中化合物2,8~10为首次从该属植物中分离得到,化合物2,5,8~10,12,14为首次从该植物中分得。并对所分得量较大的5个化合物进行了抗乳腺癌转移活性筛选,其中化合物4,11,12表现出较强的活性。  相似文献   
4.
体外转染KISS-1基因对BGC-823细胞增殖能力的影响   总被引:2,自引:2,他引:0  
目的观察KISS-1基因对人胃腺癌细胞株BGC-823增殖能力的影响,探讨KISS-1基因作为胃癌基因治疗靶点的可行性。方法利用脂质体介导在体外将KISS-1基因转染人胃腺癌BGC-823细胞,经G418筛选,建立稳定高表达KISS-1蛋白的细胞系,蛋白印迹(Western blotting)和逆转录聚合酶链反应(RT-PCR)方法证实转染成功,四甲基偶氮唑盐比色(MTT)实验探讨KISS-1对胃癌细胞株BGC-823增殖能力的影响。结果 Western blotting和RT-PCR结果显示KISS-1蛋白和mRNA在转基因组的表达均高于转空质粒组和对照组(P<0.05);MTT检测结果显示转基因组细胞在转染48 h和72 h后细胞增殖能力与转空质粒组和对照组相比,细胞生长受到明显抑制(P<0.05)。结论 KISS-1基因可抑制人胃腺癌细胞株BGC-823细胞的增殖能力。  相似文献   
5.
Laminin(LN)isamajornoncollagenousglycoproteininbasementmembranesIthasbeenreportedthatLNcouldaffectanumberofbiologicbehaviorsofcarcinomacellsmediatedbytheLNreceptors1 ItisknownthattheNlinkedcomplextypecarbohydratechainsonLNareinvolvedintherecognitionan…  相似文献   
6.
目的:研究配体结构对NAMI衍生物的水解、溶液稳定性的影响。方法:制备了化合物1 trans-[RuCl4(DMSO)(ni-ca)]Na.2DMSO(nica,nicotinamide烟酰胺);用紫外分光光度法研究了化合物1的水解机制,动力学及溶液稳定性。结果:与NAMI相似,化合物1在pH 7.40的缓冲液中发生2步脱氯水解反应(Ⅰ氯水解及Ⅱ氯水解);在pH 5.00缓冲液中二甲基亚砜(DM-SO)水解。测定了各水解反应表观速率常数、半衰期及溶液稳定性参数。结论:化合物1在酸性溶液中的稳定性明显高于中性溶液。用烟酰胺取代咪唑环能够明显减慢NAMI衍生物的脱氯水解反应速度,但对脱DMSO水解反应影响较小。  相似文献   
7.
Steps in tumor metastasis: new concepts from intravital videomicroscopy   总被引:28,自引:0,他引:28  
Summary Metastases are responsible for the majority of failures in cancer treatment. Clarifying steps in metastasis and their molecular mechanisms will be important for the development of anti-metastasis therapeutic strategies. Considerable progress has been made in identifying molecules involved in metastasis. However, because of the nature of assays that have been available, conclusions about steps in metastasis and their molecular bases have been drawn primarily from inference. In order to complete the picture of how metastases form, a technique is needed to directly watch the processin vivo as it occurs over time. We have developed an intravital videomicroscopy (IVVM) procedure to make such observations possible. Results from IVVM are providing us with new conceptual understanding of the metastatic process, as well as the nature and timing of the contributions of molecules implicated in metastasis (e.g. adhesion molecules and proteinases). Our findings suggest that early steps in metastasis, including hemodynamic destruction and extravasation, may contribute less to metastatic inefficiency than previously believed. Instead, our results suggest that the control of post-extravasation growth of individual cancer cells is a significant contributor to metastatic inefficiency. Thus, this stage may be an appropriate target for design of novel strategies to prevent metastases.  相似文献   
8.
异甘草素与光甘草定抗肿瘤转移作用比较   总被引:1,自引:1,他引:0  
目的:观察异甘草素和光甘草定对肿瘤细胞体外迁移能力以及血管内皮细胞管腔形成能力的影响,比较2种药物的抗肿瘤转移能力.方法:以20,40,60,80,100,120μmol·L-异甘草素和光甘草定作用于小鼠黑色素瘤B16F1细胞和血管内皮细胞(ECV304),干预48 h,磺酰罗丹明B(SRB)法检测细胞增殖.划痕实验评价B16F1和ECV304细胞体外迁移能力,明胶酶电泳和酶联免疫法(ELISA)测基质金属蛋白酶-2(MMP-2)的活性和表达量,吖啶橙/溴化乙锭(AO/EB)双荧光染色以及血管内皮细胞管腔样结构形成实验评价血管新生能力.结果:异甘草素和光甘草定均能显著抑制B16F1细胞和ECV304细胞增殖,且呈明显的剂量依赖性,但光甘草定对B16F1细胞的抑制率低于异甘草素.80 μmol·L-时,异甘草素与光甘草定的愈合面积分别为19.1%和27.2%,与对照组比较均有显著性差异(P<0.05),药物组与对照组相比均能降低基质金属蛋白酶-2(MM P-2)分泌与表达,药物组能显著降低血管内皮细胞迁移和管腔形成能力.光甘草定对B16F1细胞迁移,MMP-2分泌与表达,以及对ECV304细胞官腔形成的抑制能力低于异甘草素.结论:异甘草素和光甘草定都均具有抗肿瘤转移活性,80μmol·L-时,光甘草定抗肿瘤转移作用弱于异甘草素.  相似文献   
9.
 目的 观察中肺合剂对小鼠Lewis肺癌抗肿瘤肺转移的作用,并探索其相关机制。方法 采用Lewis肺癌移植瘤C57BL/6小鼠模型观察中肺合剂抗肿瘤肺转移作用,并采用荧光定量QRT-PCR法测定中肺合剂对Lewis肺癌小鼠肿瘤组织基质金属蛋白酶(MMP)-9表达的影响,采用EnVision法检测肿瘤组织血管内皮细胞生长因子(VEGF)和CD34蛋白的表达情况,并计数微血管密度(MVD)。结果 中肺合剂低、中、高剂量组(12.7,25.4,50.8 g·kg-1)和环磷酰胺(CTX)阳性对照组对移植性Lewis肺癌小鼠的肺转移抑制率为16.7%、45.8%、19.4%和80.6%,以中剂量组肺转移抑制作用最佳。中肺合剂能下调Lewis肺癌小鼠肿瘤组织MMP-9、VEGF蛋白的表达水平,并降低肿瘤组织MVD。MMP-9、VEGF表达和MVD之间呈正相关。结论 中肺合剂对小鼠Lewis肺癌具有显著的抗肿瘤肺转移作用,以中剂量组最佳。其作用机制可能与该药能降低肿瘤组织MMP-9、VEGF蛋白的表达水平,并降低肿瘤组织MVD有关。  相似文献   
10.
Objective To further study the anti-metastasis mechanism of laminin-glycopeptides on carcinoma cell proliferation, apoptosis and the secretion of matrix metalloproteinases. Methods Human hepatocellular carcinoma cells in serum free medium were incubated on laminin-coated substrate with or without laminin-glycopeptides at a final concentration of 50 μg/ml. The total number of surviving cells after incubating for the indicated time was assayed by MTT assay. DNA synthesis of the incubated cells was detected by (3)H-TdR incorporation.Cell cycle was analysed by FACS.The mitotic index of Giemsa stained cells was assessed.Cell apoptosis was detected by both FACS and an acridine orange staining method.Matrix metalloproteinase secretion was analysed by gelatin zymography. Results The total number of surviving cells incubated on laminin in the absence of laminin-glycopeptides was significantly larger than that in the presence of laminin-glycopeptides. Laminin promoted (3)H-TdR incorporation of carcinoma cells, decreased the percentage of cells in G1 phase and increased the percentage of cells in S phase.In contrast, laminin-glycopeptides could inhibit the effect of laminin as shown by (3)H-TdR incorporation and cell cycle analysis. The percentage of cells in G2+M phase and the mitotic index among various groups showed no significant difference.Matrix metalloproteinases secretion from cells treated by laminin-glycopeptides was much less compared to that without the treatment by laminin-glycopeptides. Conclusion Laminin may stimulate cell proliferation, while laminin-glycopeptides could significantly inhibit the effect of laminin by inhibiting DNA synthesis and arresting the carcinoma cell cycle from G1 to S phase.These effects may inhibit not only tumor growth of the primary carcinoma, but also the establishment of metastases at ectopic tissues. Laminin-glycopeptides could also inhibit the secretion of matrix metalloproteinases from carcinoma cells and this may contribute to their decreased invasive and metastatic phenotype. This study further revealed the cellular and molecular mechanism of laminin-glycopeptides on anti-metastasis.  相似文献   
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