基于DSPE-PEG-PDP的靶向纳米载体构建及其在基因递送中的应用研究
专著:系统阐述脂质体崩裂的驱动安装力:外界扰动和化学工业判断力外部链接://pubs.acs.org/doi/abs/10.1021/la300127m编辑:王曦,马修·M·辛德尔,王思文,雷吉娜·拉根英文论文:在反义寡脱氧核苷酸 (AS-ODN) 或小抑制性 RNA (siRNA) 物理辽法使用选择猿类基因抑制性现已*中国传统口服药物难以医好的症状。当然,反义物理辽法原因在生理学液中的平衡性能差和細胞内摄食有限公司而会受到的阻碍。要解决方法此类的问题,我们公司实践室激发了种配体靶向疗法药物和面积平衡的微米颗粒剂药制剂。猿类1.肺癌細胞大部分过表示 σ 感觉,由于可不可以用当前配体(举例子茴香酰胺)使用靶向疗法药物*。将而对猿类能素的 AS-ODN 或 siRNA 与的载体 DNA(大牛胸腺 DNA)搭配,并且与鱼精球蛋白(属于带高正自由电荷的肽)包覆。将增值税离子用由 DOTAP 和甘油三酯(摩尔比 1:1)组合的阳亚铁化合物脂质体包被,以得到 LPD(脂质体-聚阳亚铁化合物-DNA)納米离子。其次,进行后加上法将现浇混凝土的LPD納米离子与DSPE-PEG-茴香酰胺(我们公司进行实验所早联合开发的另一种PEG化配体脂质)在一块孵育,产生配体靶点性和空间区域稳固性。一起准备了DSPE-PEG发泡密封条的非靶点納米离子做对应。能够Survivin mRNA调低、Survivin蛋白酶调低、引起*组织凋亡的程度、*组织产生调控各种处置后的*组织对*癌制剂的电学增敏影响来检验nm技术技术离子的反义活力性。我国感觉,PEG化nm技术技术离子的*组织递送和反义活力性是队列依懒性的,从而依懒于茴香酰胺配体的长期存在。靶向治疗治疗PEG化nm技术技术离子对寡核苷酸的摄取量能够会被过多会的矿酸配体价格竞争。我国的没想到表示,配体靶向治疗治疗和面积安稳的nm技术技术离子会选性地将 AS-ODN 和 siRNA 递送去肺腺癌组织中做好*。AbstractAbstract ImageAtomic force microscopy (AFM) studies under aqueous buffer probed the role of chemical affinity between liposomes, consisting of large unilamellar vesicles, and substrate surfaces in driving vesicle rupture and tethered lipid bilayer membrane (tLBM) formation on Au surfaces. 1,2-Distearoyl-sn-glycero-3-phosphoethanolamine-N-poly(ethylene glycol)-2000-N-[3-(2-pyridyldithio) propionate] (DSPE-PEG-PDP) was added to 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) vesicles to promote interactions via Au–thiolate bond formation. Forces induced by an AFM tip leading to vesicle rupture on Au were quantified as a function of DSPE-PEG-PDP composition with and without osmotic pressure. The critical forces needed to initiate rupture of vesicles with 2.5, 5, and 10 mol % DSPE-PEG-PDP are approximately 1.1, 0.8, and 0.5 nN, respectively. The critical force needed for tLBM formation decreases from 1.1 nN (without osmotic pressure) to 0.6 nN (with an osmotic pressure due to 5 mM of CaCl2) for vesicles having 2.5 mol % DSPE-PEG-PDP. Forces as high as 5 nN did not lead to LBM formation from pure POPC vesicles on Au. DSPE-PEG-PDP appears to be important to anchor and deform vesicles on Au surfaces. This study demonstrates how functional lipids can be used to tune vesicle–surface interactions and elucidates the role of vesicle–substrate interactions in vesicle rupture.



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