含强弱可逆双配位键的仿生力诱导本征自修复高分子材料

The present project is focused on development of intrinsic self-healing polymer capable of functioning upon cracking under applied stress without manual intervention. To this end, we are going to mimic byssus of mussels and introduce strong and weak coordination bonds into polyurethane building up dual reversibly crosslinked networks. When the weak coordination bonds preferentially rupture, the surrounding micron-environment would change accordingly, leading to the increase of the amount of the strong coordination bonds. As a result, stress induced strengthening occurs, which hinders crack propagation. In the case of unloading, the strong coordination bonds favor rebound of the macromolecular chains and crack closure. By taking advantage of specificity of coordination bonds, the broken weak coordination bonds would be gradually reconnected and the number of the strong coordination bonds would also be recovered in the meantime. The joint action of the reversible cleavage-formation of both strong and weak coordination bonds realizes rearrangement of the crosslikages and crosslinked networks, and rebinds cracks. On the basis of molecular design, synthesis of the above-mentioned polyurethane containing the two types of reversible crosslinkages, and study of reversibility of the coordination bonds in relation to macromolecular structure and material’s properties, the influences of polymer synthesis, fabrication, dynamic reversible breakage-recombination of the dual coordination bonds on healing efficiency and stress modulated response would be revealed. Eventually, the difficulties of manually aided intrinsic self-healing and the unstable autonomic intrinsic self-healing would be overcome. The outcomes of this project would provide a knowledge path for future development of bio-inspired stress-induced intrinsic self-healing polymers.

为在高分子材料受力破坏的同时引发其本征自修复机制，从而进行无人工干预、自动愈合微损伤，我们拟模仿贻贝足丝，在聚氨酯中引入强、弱两种配位键形成双可逆交联网络，利用弱配位键在外力下率先破坏时改变分子周边的微环境，导致强配位键数量的增加，产生应力增强、抑制裂纹发展，卸去外力时，由于强配位键促进分子链回缩和裂纹闭合，加上配位键的特异性作用，弱配位键重新形成，强配位键数也逐渐回复。这种强弱配位键可逆形成与破坏的有机结合，可实现网络结构和强弱交联键分布的重排，修复微损伤。通过设计分子和网络结构，合成含上述双可逆交联键的聚氨酯，研究配位键可逆特性与分子结构和材料性能的关系，揭示材料合成、制备技术、双配位键断裂—结合动态可逆行为对修复效率和力调控响应的影响；阐明力诱导本征自修复过程，克服现有本征型自修复高分子材料多需人工干预或无需人工干预却性能不稳定的困难，为构筑仿生力诱导自修复高分子材料建立科学基础。

高分子材料在工农业和人类日常生活中得到广泛应用，在使用过程中高分子材料由于机械疲劳、热疲劳、冲击、辐射、化学降解等作用不可避免地会在其内部产生局部损伤和微裂纹，导致性能下降。因此，对高分子材料微裂纹的早期发现和修复是一个非常实际的问题，由于聚合物的裂纹往往在其内部深处出现，很难采用常规手段探测，并且即便能够探测得到，也无法修复。因此，研究赋予高分子材料类似生物体的仿生修复-自愈合能力，主动、自动地对损伤部位进行修复、对高分子材料的应用十分重要。. 为在高分子材料受力破坏的同时引发其本征自修复机制，从而进行无人工干预、自动愈合微损伤，本项目模仿贻贝足丝，在聚氨酯中引入多巴与铁（DOPA-Fe）以及组氨酸与锌（His-Zn）强、弱两种配位键形成双可逆交联网络，利用弱His-Zn配位键在外力下率先破坏时释放出咪唑环，增加了体系的碱性,改变分子周边的微环境，导致强配位键（DOPA-Fe三配位键）数量的增加，产生应力增强、抑制裂纹发展；卸去外力时，由于DOPA-Fe强配位键促进分子链回缩和裂纹闭合，加上配位键的特异性作用，原本受力断裂的弱键（His-Zn键）重新结合，体系的碱性降低，在受力过程中新生成的强键（DOPA-Fe键）因而逐渐解开，强配位键数也逐渐回复。在此过程中，材料自动闭合并修复受力过程中产生的微裂纹，从而恢复到原来的力学状态。这种强弱配位键可逆形成与破坏的有机结合，实现了网络结构和强弱交联键分布的重排，修复微损伤。我们通过设计分子和网络结构，合成含上述双可逆交联键的聚氨酯，研究配位键可逆特性与分子结构和材料性能的关系，揭示了材料合成、制备技术、双配位键断裂—结合动态可逆行为对修复效率和力调控响应的影响；阐明力诱导本征自修复过程，克服现有本征型自修复高分子材料多需人工干预或无需人工干预却性能不稳定的困难，为构筑仿生力诱导自修复高分子材料建立了科学基础。

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