Synthesis, Crystal Structure and Inhibition of the K562 Cell Proliferation of N＇-Tertbutylaminocarbonyl-N-2-chlorophenoxyacetylthiourea

The title compound N'-tert-butylaminocarbonyl-N-2-chlorophenoxyacetylthiou- rea has been synthesized for the first time. Complete assignments were achieved by IR, 1H NHR and single-crystal X-ray diffraction analyses. The inhibitory rate of the cellular growth of K562 cells (chronic myeloid 1eukemic cells) was measured using MTT [3-(4,5-dimethylthiazo-2-y1)-2,5-di- phenyltetra-zolium bromide] assay. The cell apoptosis was assessed by agarose gel electrophoresis to find that the title compound has antiproliferation and apoptosis inducing effects on K562 cells. In order to investigate the relationship between structure and activity of the target compound, we report its crystal structure and biological behavior in the present paper. Crystallographic data: C14H18- ClN3O3S, Mr = 343.82, orthorhombic, space group Pnma, a = 19.786(6), b = 6.789(2), c = 12.938(4) , V = 1738.0(9) 3, Z = 4, Dc = 1.314 g/cm3, F(000) = 720, μ(MoKα) = 0.354 mm-1, R = 0.0378 and wR = 0.0941. The molecule is a planar structure.     

骨髓基质干细胞在等离子体处理PEGDA基凝胶表面的黏附和增殖

通过低温等离子体技术对聚乙二醇双丙烯酸酯(PEGDA)/甲基丙烯酸β-羟乙酯(HEMA)共聚物水凝胶生物材料进行表面改性,以骨髓基质干细胞(BMSc)为细胞模型,考察了细胞在等离子体表面改性前后的水凝胶材料的黏附和增值行为,材料的表面性能通过 X 射线光电子能谱、接触角和扫描电镜进行表征.研究结果表明,材料表面经氩等离...     

Treatment activity of a mixed-ligand coordination polymer on gastric carcinoma

Reaction of 4,4′,4″-nitrilotribenzoic acid (H₃L), a C₃-symmetric ligand, with the divalent Co(II) salt Co(NO₃)₂·6H₂O in the present of the N-donor ligand 1,2-di(4-pyridyl)ethylene (DPE) affords a new mixed-ligand coordination polymer with the chemical formula of [Co₃(TNB)(DPE)₂]·2H₂O·DMF (1). In this study, CCK-8 assay was used to determine the effect of novel compound on proliferation of gastric cancer cells. The VEGF signaling pathway in gastric cancer cells was determined through employing real-time PCR after treatment of the above complex. Further, molecular docking simulation confirmed that the biological activity was coming from the carboxyl groups through the hydrogen bonding interactions with the receptor protein, the pyridine group only bonded with the Co ion for the formation of the Co complex.     

PRLs Promote Spreading, Adhesion, and Proliferation of Human SW480 and SW620 Cells

IntroductionMetastasis is the leading cause of the death ofcancer patients.It represents a complex and multi-stepprocess including the detachment of tumor cells from aprimary cancer,the invasion into the surrounding tis-sue,the entry into the circulatory system,the reinva-sion,and the proliferation at a distant secondarysite[1,2].A wide variety of stimuli are known to be as-sociated with the metastasis of tumor cells,which in-clude cytokines,hormones,growth factors,and extra-cellular matrix pr…     

MicroRNA-143对人乳腺癌MCF-7细胞侵袭和迁移的影响

目的探讨microRNA-143（miR-143）对人乳腺癌MCF-7细胞侵袭、迁移和增殖的影响。方法在脂质体介导下将miR-143抑制剂（miR-143 inhibitors）转染入MCF-7细胞，以inhibitor negative control（inhibitor NC）作为阴性对照。通过MTS试剂盒检测细胞增殖能力，以Transwel 侵袭实验和迁移实验分别检测细胞侵袭能力和迁移能力。结果（1）miR-143 inhibitors组与inhibitor NC组间细胞增殖活性无明显差异（P＞0.05）；（2）Transwel 侵袭及迁移实验显示转染miR-143 inhibitors后，MCF-7细胞的侵袭及迁移能力均明显增强（P＜0.05）。结论 miR-143对人乳腺癌MCF-7细胞的侵袭及迁移能力存在负性调控作用，可能成为乳腺癌治疗的潜在靶点。     

吉西他滨联合槲皮素对胰腺癌细胞Panc-1凋亡的影响研究

目的研究吉西他滨联合槲皮素抑制胰腺癌细胞Panc-1增殖,促进其凋亡的效果.方法设立槲皮素(终浓度为50μM)、吉西他滨(50μg/ml)、吉西他滨联合槲皮素和对照组4组,MTS法检测药物对Panc-1细胞凋亡的影响,流式细胞仪检测联合药物处理对细胞凋亡和细胞周期的影响,最后应用荧光定量PCR法测定凋亡相关基因BCL-2家族蛋白的相对表达.结果吉西他滨联合槲皮素后,对胰腺癌促凋亡效果增强,同时改变细胞周期,使其S期减少,BCL-2家族促凋亡基因表达上调.结论槲皮素能够显著增强吉西他滨抑制胰腺癌恶性增殖的作用.     

Taurine Inhibits Myocardial Fibrosis via PKC-ERK1/2 Signaling Pathways

Previous studies have demonstrated the important role of taurine in inhibiting proliferation of myofibroblasts( myoFb) and myocardial fibrosis. However, the underlying mechanisms are unclear. The present study was designed to shed light on this issue through exploring the signal pathways via in vitro experiments. Angiotension Ⅱ (AngⅡ) treatment significantly increased myoFb proliferation and the levels of collagens Ⅰ and Ⅲ(P<0.05), whereas taurine, PKCα(PKC: protein kinase C) specific inhibitor L-threo-dihydro-sphingosine(D4681), ERK1/2 inhibitor (PD98095) abrogated myoFb proliferation and collagen levels(P<0.05, P<0.01, respectively), and increased the G₀/G₁ phase rate and decreased S phase rate. Immunocytochemistry, confocal fluorescence staining and image analysis showed that taurine could inhibit the translocation and expression of p-PKCαin membrane, and then inhibit nuclear translocation and expression of p-ERK1/2. These results have statistically significant differences compared with those of AngⅡ group(P<0.01). Western blot results also show that taurine could inhibit the protein expression of p-PKCα and p-ERK1/2. We used p-PKCα specific inhibitor D4681 in order to elucidate the relationship between p-PKCα and p-ERK1/2 in signal transduction pathways. Finally, the results show that the protein expression of p-ERK1/2 and nuclear translocation were suppressed in D4681 group.     

乙烯基桥联的8-羟基喹啉衍生物的合成、抗氧化活性及促进鼠骨髓间质干细胞增殖的研究

设计合成了2-乙烯基取代的8-羟基喹啉衍生物(6), 用IR, UV-Vis, 1H NMR, MS和元素分析确认其结构; 利用二苯代苦味酰基自由基(DPPH·)法和噻唑蓝比色(MTT)法分别测定了目标产物的抗氧化活性及调控鼠骨髓间质干细胞(MSCs)增殖的作用. 结果表明, 目标产物有较强的抗氧化活性, 随着产物浓度的增加, 其抗氧化活性先增强后减弱; 在低浓度时对鼠骨髓间质干细胞有促进作用. 研究发现, 化合物6抗氧化活性的提高与其含量相关.     

线性调控分枝过程的若干结果

本文给出了调控函数 φ(x) =kx b的在零点停止的线性调控分枝过程的增殖速度 ,证明了过程的不稳定性 ,得到了当b =0时成员总数wn 的概率母函数所满足的方程 .     

Effect of poly(hydroxybutyrate-co-hydroxyhexanoate) microparticles on growth of murine fibroblast L929 cells

Poly(hydroxybutyrate-co-hydroxyhexanoate) (PHBHHx) microparticles were successfully prepared and their proliferative effects on cultured fibroblasts were studied. PHBHHx microparticles (0.005-0.1 g/L) promoted cell proliferation in murine fibroblast L929 and elevated intracellular calcium concentrations ([Ca²⁺]_i). EGTA (ethylene glycol-bis(2-aminoethylether)-N,N,N′,N′-tetraacetic acid) inhibited PHBHHx microparticle-induced cell proliferation by chelating the extracellular Ca²⁺ and blocking the PHBHHx particle-induced [Ca²⁺]_i increase. Transwell experiments demonstrated that PHBHHx microparticles stimulated fibroblast proliferation when separated from cells by a 0.4 μm filter as effectively as when applied directly to cells. Since PHBHHx microparticles had a diameter of 75 μm, the stimulatory effect of PHBHHx particles on cell growth was attributed to degradation products smaller than 0.4 μm in diameter. The trophic effect of these microparticles is consistent with our previous reports demonstrating good biocompatibility for PHBHHx.