Immobilizing argatroban and mPEG-NH2 on a polyethersulfone membrane surface to prepare an effective nonthrombogenic biointerface
Immobilizing argatroban and mPEG-NH2 on a polyethersulfone membrane surface to prepare an effective nonthrombogenic biointerface
复制标题
将阿加曲班和 mPEG-NH2 固定在聚醚砜膜表面制备有效的非血栓生物界面
DOI：
10.1080/09205063.2019.1595891
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发表时间：
2019-04-03
影响因子：
3.6
通讯作者：
Ning, Jianping
中科院分区：
文献类型：
--
作者：
Dai, Yanling;Dai, Siyuan;Ning, Jianping
摘要临床上血液透析(HD)患者出血风险高，不宜采用全身抗凝治疗。提供局部抗凝膜表面的HD膜可能是解决HD患者这一棘手问题的一种有前途的策略。在这里，我们通过聚多巴胺(PDA)策略，通过接枝阿加曲班(AG)和甲氧基聚乙二醇胺(mpeg-NH2)来修饰非血栓形成的聚醚砜(PES)透析膜。将聚乙二醇单甲醚底物在碱性多巴胺溶液中浸泡24 h，然后将AG和mpeg-nH2依次接枝到所形成的膜上。利用衰减全反射傅里叶变换红外光谱(ATR-FTIR)和X射线光电子能谱(XPS)对PDA的引入以及AG和MPEGNH_2的固定化进行了表征。用扫描电子显微镜(SEM)和原子力显微镜(AFM)观察了表面改性后的表面结构和形貌。通过抑制血小板黏附和活化、延长凝血时间、抑制凝血酶生成和补体激活，证明了改性膜具有良好的抗血栓形成能力。这项工作描述了一种有效和方便的方法来固定化AG和mpeg-NH2，以创建用于血液接触设备(如HD膜)的非血栓形成生物界面。
Abstract Systemic anticoagulation is not suitable for hemodialysis (HD) patients with a high risk of bleeding in the clinic. An HD membrane that provides a localized anticoagulation membrane surface may be a promising strategy to solve this intractable problem for HD patients. Herein, we modified a nonthrombogenic polyethersulfone (PES) dialyzer membrane by grafting argatroban (AG) and methoxy polyethylene glycol amine (mPEG-NH2) via a polydopamine (PDA) strategy. The PES substrates were immersed in an alkaline dopamine solution for 24 h, and then, AG and mPEG-NH2 were sequentially grafted covalently onto the resultant membrane. Attenuated total reflection-Fourier transform infrared spectroscopy (ATR-FTIR) and X-ray photoelectron spectroscopy (XPS) were utilized to confirm the successful introduction of PDA and the immobilization of AG and mPEG-NH2. Scanning electron microscopy (SEM) and atomic force microscopy (AFM) were used to observe the surface structure and morphology after the surface modification. The excellent antithrombotic abilities of the modified membrane were demonstrated by the suppression of platelet adhesion and activation, prolongation of clotting times, and inhibition of thrombin generation and complement activation. This work describes an efficient and convenient method to immobilize AG and mPEG-NH2 to create a nonthrombogenic biointerface for blood-contacting devices such as HD membranes.