1Department of Biomedical Engineering, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan.
J Biomater Appl. 2013 Nov;28(4):544-51. doi: 10.1177/0885328212462260. Epub 2012 Oct 9.
Four different dynamic biomaterial surfaces with different molecular architectures were prepared using two hydrophilic polymers: poly(ethylene glycol) and polyrotaxanes containing α-cyclodextrin. Either one or both terminals of the poly(ethylene glycol) or polyrotaxanes were immobilized onto a gold substrate via Au-S bonds, resulting in poly(ethylene glycol)-graft, polyrotaxanes-graft, poly(ethylene glycol)-loop, and polyrotaxanes-loop structures. Human platelet adhesion was suppressed more effectively on the graft surfaces than on the loop surfaces for both poly(ethylene glycol) and polyrotaxanes due to the high mobility of graft polymer chains with a free terminal. Moreover, the platelets adhered to the polyrotaxane surfaces much less than the poly(ethylene glycol) surfaces, possibly because of the mobile nature of the α-cyclodextrin molecules that were threaded on the poly(ethylene glycol) chain. Actin filament assembly in adherent platelets was also greatly prevented on the poly(ethylene glycol)/polyrotaxanes-graft surfaces in comparison with the corresponding loop surfaces. A clear correlation between the numbers and areas of adherent platelets on these surfaces suggests that platelet adhesion and activation were dominated by the platelet GPIIb/IIIa-adsorbed fibrinogen interaction. These results indicate that both of the different modes of dynamic features, sliding/rotation of α-cyclodextrin and polymer chain mobility, effectively suppressed platelet adhesion in spite of the similar hydrophilicity. This research affords a novel chemical strategy for designing hemocompatible biomaterial surfaces.
聚乙二醇和含有α-环糊精的聚轮烷制备的。聚乙二醇或聚轮烷的一端或两端通过 Au-S 键固定在金基底上,形成聚乙二醇接枝、聚轮烷接枝、聚乙二醇环和聚轮烷环结构。由于接枝聚合物链的末端自由,因此与聚乙二醇和聚轮烷的环表面相比,血小板在接枝表面上的黏附受到更有效的抑制。此外,由于α-环糊精分子在聚乙二醇链上的可移动性,血小板黏附在聚轮烷表面上的程度远低于聚乙二醇表面。与相应的环表面相比,在聚乙二醇/聚轮烷接枝表面上,黏附的血小板中的肌动蛋白丝组装也被大大抑制。与这些表面上黏附的血小板数量和面积之间存在明显的相关性表明,血小板黏附和激活主要受血小板 GPIIb/IIIa 吸附纤维蛋白原的相互作用控制。这些结果表明,尽管亲水性相似,但两种不同的动态特征模式,即α-环糊精的滑动/旋转和聚合物链的移动,都能有效地抑制血小板黏附。这项研究为设计抗凝血生物材料表面提供了一种新的化学策略。