Sojucktang induces apoptosis via loss of mitochondrial membrane potential and caspase-3 activation in KLE human endometrial cancer cells

Sojucktang （SJT） has long been used for the treatment of endometrial diseases in Korea. However, the mechanisms responsible for the SJT-induced apoptosis in endometrial cancer cells remain unclear. In the present study, SJT was demonstrated to show cytotoxic effect and induce apoptotic cell death via mitochondrial regulation in KLE endometrial cancer cells. Linderae Radix, Glycyrrhizae Radix, Zedoariae Rhizoma, Trogopterorum Faeces and Agelicae Gigantis Radix were found to be the potent constituent herbs of SJT to significantly decrease the viability of KLE cells by a tetra zolium salt （XTT） assay. Apoptotic bodies were observed in SJT-treated KLE cells by 4′-6-diamidino-2-phenylindole （DAPI） and TdT-mediated-dUTP nick-end labeling （TUNEL） assay. SJT also increased sub-G1 DNA contents of the cell cycle undergoing apoptosis in a dose-dependent manner. Furthermore, it was observed that SJT activated caspase-3 and cleaved poly （ADP-ribose） polymerase （PARP）, and decreased mitochondrial membrane potential in a dose-dependent manner. Taken together, this study shows that SJT exerts anti-tumor activity against KLE endometrial cancer cells via mitochondrial dependent apoptosis induction.     

Role of FGF-2／FGFR signaling pathway in cancer and its signification in breast cancer

Fibroblast growth factor-2 (FGF-2) is a member of a large family of proteins that bind heparin and heparan sulfate and modulate the function of a wide range of cell types. It has been proved that FGF-2 stimulates the growth and development of new blood vessels (angiogenesis) that contribute to the pathogenesis of several diseases (i.e. cancer, atherosclerosis). However, many of the biological activities of FGF-2 have been found to depend on its receptor抯 intrinsic tyrosine kinase activity and second messengers such as the mitogen activated protein kinases. This review will focus on the mechanism of FGF-2/FGFR induced signaling pathway in tumor and human breast cancer.     

硒诱导肿瘤细胞凋亡的实验研究

目的：研究硒抑制肿瘤细胞生长的机理。方法：采用DNA电泳及流式细胞仪分析等方法。结果：硒能诱导Hela细胞调亡。1．5％琼脂凝胶电泳呈现典型的阶梯现象。流式细胞仪检测显示大量的亚二倍体细胞。结论：硒促进Hela。肿瘤细胞凋亡,可能是硒抑制肿瘤细胞生长的机理之一。     

Rapid senescence induced by overexpression of p53 in NIH3T3 cells

An NIH3T3 cell line which overexpresses temperature-sensitive p53Val135 was constructed by introduction of p53Val135 gene. It exhibited rapidly characteristic morphological and biochemical alterations related to repli-cative senescence when being cultured in 32℃. We suggested that the overexpression of p53 activated probably the onset of senescence in NIH3T3 cells, which induced a rapid cellular senescence.     

Apoptosis induced by （DIPP-L-Leu）2-L-Lys-OCH3 in K562 cells

Apoptosis as a mechanism of deleting cells from tissues plays an important role in physiological and varieties of pathological situations, especially cancer conditions. In order to search for tumor cells apoptosis inducers, the inhibition effects on K562 cells of N-phosphoryl dipeptide methyl esters were studied by MTT assays, and (DIPP-L-Leu)2-L-Lys-OCH3 was the compound which had the best activity. From the studies of the typical apoptotic morphologic changes, DNA agarose gel electrophoresis, and flow cytometry analysis, it could be concluded that (DIPP-L-Leu)2-L-Lys-OCH3 could induce apoptosis of K562 cells in a dose-dependent manner, and the IC50 was 22.66 μmol/L according to MTT assays.     

CPUY013对胰腺癌Capan2的生长抑制与诱导凋亡作用

探讨CPUY013对体外培养人胰腺癌细胞Capan2生长抑制及诱导凋亡作用.采用MTT法、克隆原形成法检测CPUY013对Capan2细胞生长的抑制作用,采用流式细胞仪分析CPUY013对细胞周期的影响,Western Blot法检测TopoⅠ、野生型p53、caspase-3、bcl-2和bax蛋白表达的变化.MTT法、集落形成试验结果显示,CPUY013对体外培养的人胰腺癌细胞Capan2有明显的生长抑制作用,处理72 h的IC50值为7.3×10^-7mol/L（MTT法）,CPUY013在8.0×10^-8mol/L浓度可以明显抑制Ca-pan2细胞的集落形成,抑制率为69.6%.同时,CPUY013可剂量依赖地降低Capan2细胞G1期细胞的比例,升高S期细胞的比例,呈现明显的S期阻滞.CPUY013可下调TopoⅠ蛋白的表达,上调细胞中p53、caspase-3、bax蛋白表达,下调bcl-2蛋白表达,并呈剂量依赖性.CPUY013对Capan2细胞具有明显的生长抑制作用,阻滞细胞周期进程,诱导Capan2细胞凋亡,其可能与降低细胞内TopoⅠ蛋白表达,增加p53、caspase-3、bax蛋白表达,降低bcl-2蛋白表达有关.     

刺老苞根皮黄酮对H_2O_2诱导的MC3T3-E1成骨细胞损伤改善

在H2O2胁迫下,研究刺老苞根皮(Aralia echinocauIis)黄酮增强MC3T3-E1成骨细胞抗自由基损伤的作用.为此用H2O2作用MC3T3-E1成骨细胞,建立自由基损伤细胞模型.培养的成骨细胞分为对照组、模型组、刺老苞根皮黄酮低剂量组(1×10-8mol/L)、刺老苞根皮黄酮中剂量组(1×10-7mol/L)和刺老苞根皮黄酮高剂量组(1×10-6mol/L).测定不同处理组细胞活力、超氧化物歧化酶(superoxide dismutase,SOD)活性、活性自由氧(reactive oxygen species,ROS)含量、脂质过氧化物(lipid oxygen,LPO)含量,同时利用荧光偏振法测定细胞膜流动性.结果显示与模型组相比,刺老苞根皮黄酮组细胞活力、SOD活性、细胞膜流动性均显著升高(P<0.01),而ROS含量、LPO含量则显著降低(P<0.01),并呈现一定的量效关系.可以认为H2O2摄入会导致MC3T3-E1成骨细胞的氧化损伤,而刺老苞根皮黄酮可以预防或降低此类损伤对细胞的影响.     

Si和Al对机械合金化合成Ti_3SiC_2的影响

采用3Ti/Si/2C单质粉体为原料,进行机械合金化,以合成Ti3SiC2粉体.研究了Al和过量Si对机械合金化合成Ti3SiC2的影响.研究结果表明,机械合金化单质混合粉体,会诱发自蔓延反应.反应后产生大量坚硬的颗粒状产物.机械合金化3Ti/Si/2C粉体,会产生组成相为TiC、Ti3SiC2、TiSi2和Ti5Si3的粉体与颗粒产物.添过量Si并不会促进机械合金化反应合成Ti3SiC2.添适量Al可消除硅化物,明显促进反应合成Ti3SiC2.采用3Ti/Si/2C/0.15A1粉体作原料时,颗粒产物中Ti3SiC2含量最高,为92.8wt%;而采用3Ti/Si/2C/0.20A1粉体作原料时,粉体产物中Ti3SiC2含量最高,为61.9wt%.     

As2S3纳米粒的制备及其对肝癌SMMC-7721细胞的治疗作用

研究了雌黄纳米粒的制备方法及其抗肿瘤作用.采用化学方法制备A s2S3纳米粒,通过透射电镜、X射线能谱(EDS)对A s2S3纳米粒进行分析表征,以形态学、MTT法和流式细胞术体外研究不同浓度的A s2S3纳米粒对肝癌SMMC-7721细胞生长的影响,并同时与传统剂型的A s2S3进行比较.分析结果显示:实验制备的A s2S3纳米粒平均直径约为80nm,电镜下呈圆形,大小较一致,分散性较好,EDS证实其为A s2S3,无其他成分;A s2S3纳米粒对SMMC-7721细胞有明显的生长抑制和凋亡诱导作用,且呈浓度和时间依耐性,其细胞生长抑制率和凋亡诱导率明显高于相同浓度传统剂型的A s2S3处理组(p<0.001).表明化学法可以制备A s2S3纳米粒;与传统剂型的A s2S3相比,A s2S3纳米粒有更强的抗肿瘤作用.     

2-ME抑制人子宫内膜癌细胞株增殖的研究

目的　探讨2-甲氧雌二醇(2-ME)对人子宫内膜癌细胞株KLE细胞体外增殖和凋亡的抑制作用.方法选用人子宫内膜癌细胞株KLE进行体外培养,实验组加入不同浓度2-ME的培养液,对照组不含2-ME.用四甲基偶氮唑蓝(MTT)比色法观察2-ME对人子宫内膜癌细胞株KLE增殖的抑制作用;药物作用后的克隆形成实验;电子显微镜(电镜)观察细胞形态变化;流式细胞仪(FCM)观察细胞的凋亡率及细胞周期的变化.结果2-ME浓度为10.0～50.0μM时,明显抑制KLE细胞的增殖(P<0.01),并具有时间依赖性和剂量依赖性.2-ME作用后G0/G1期细胞增加,并伴随G0/G1期细胞的增加,出现细胞凋亡峰和凋亡率的升高(P<0.05).电镜下观察到KLE细胞染色体边集、核固缩、凋亡小体.结论2-ME对人子宫内膜癌KLE细胞株增殖有抑制作用,并能促进其凋亡.     

具有磁感应定向加热肿瘤治疗作用的纳米As2 O3磁性脂质体的制备和表征

在薄膜法制备工艺基础上,采用反复冻融和超声处理、并加明胶分散磁性粒子的改良方法制备纳米As2O3磁性脂质体,然后应用透射电子显微镜、能谱仪、原子荧光光谱仪和图像分析系统等对其特性进行检测.结果所得纳米As2O3磁性脂质体粒径为(190±80) nm,球形或卵球形, 有一个明显磁性核心,As2O3的包封率为53.0%.所以此改良法制备出的纳米As2O3磁性脂质体粒径较小、稳定性好和药物包封率高,有可能作为一种较理想的肿瘤靶向治疗复合载体发挥药物和磁感应加热的联合定向治疗作用.     

SmCl_3-CaCl_2-MgCl_2体系相图的研究

利用差热分析方法研究了 SmCl_3-CaCl_2-MgCl_2 三元体系相图。发现它属于简单共晶型,三元共晶点E为50.0mol％SmCl_3,30.5mol％CaCl_2,528℃。     

CdCl2诱导秋粘虫细胞(Sf9)凋亡的初步研究

以秋粘虫（Spodoptera frugiperda Sf9）的细胞为材料，用不同浓度的CdCl2，通过Giemsa染色的形态学方法，研究其细胞凋亡．结果表明，在重金属离子的胁迫作用下，不同浓度的重金属离子致使细胞死亡率不同；其急性损伤域为136μmol／L；20μmol／L CdCl2作用6h后，Sf9细胞出现了凋亡小体．     

As2O3联合FP99诱导骨肉瘤细胞MG-63凋亡的初步研究

采用噻唑蓝(MTT)法发现FP99能够协同三氧化二砷(As2O3)抑制人骨肉瘤细胞MG-63的生长,并采用流式细胞计数进一步证实FP99加强As2O3对MG-63细胞凋亡的诱导作用;进而检测了Caspase-3的活性,发现As2O3联合FP99作用MG-63细胞后,Caspase-3的活性显著提高,提示我们As2O3联合FP99增加MG-63细胞的凋亡率的机制可能是通过提高Caspase-3激酶活性,从而促进了整个凋亡通路的激活,最终导致细胞凋亡的增加。     

应用KF-Al2O3作催化剂合成2-庚酮

研究了用KF-Al2O3作催化剂,正溴丁烷与乙酰乙酸乙酯的化学反应,以正丁基取代乙酰乙酸乙酯中的α-H,实现了碳-碳烷基化反应,合成了正丁基乙酰乙酸乙酯,再经水解脱羧制得2-庚酮,收率为72.5%,比常规醇钠法制得2-庚酮的收率提高了14.5个百分点.