Wu Chengwei, Duan Xiyue, He Xuzhao, Weng Wenjian, Zhou Hang, Han Gaorong, Chen Zuobing, Chen Wen, Cheng Kui
Department of Rehabilitation Medicine, the First Affiliated Hospital, School of Medicine, School of Materials Science and Engineering, National Key Laboratory of Silicon and Advanced Semiconductor Materials, Zhejiang University, Hangzhou 310027, China; Institute of Wenzhou, Zhejiang University, Wenzhou 325006, China.
Department of Rehabilitation Medicine, the First Affiliated Hospital, School of Medicine, School of Materials Science and Engineering, National Key Laboratory of Silicon and Advanced Semiconductor Materials, Zhejiang University, Hangzhou 310027, China.
Colloids Surf B Biointerfaces. 2025 Nov;255:114885. doi: 10.1016/j.colsurfb.2025.114885. Epub 2025 Jun 17.
Neuroinflammation associated with inflammatory activation of astrocytes on the interface of implanted neural electrodes is the main cause of electrode failure. In this work, collagen/polypyrrole composite film (CPF) was designed and fabricated to modify the interface. The CPF had the co-exposure of collagen and polypyrrole in morphology, which allowed the biomimetic microenvironment provided by collagen to effectively inhibit the inflammatory activation of astrocytes. Meanwhile, the polypyrrole in the composite film significantly improved the electrochemical performance of the electrode interface, enabling it to provide an electrical microenvironment that inhibited inflammatory activation of astrocytes under electrical stimulation. Moreover, mechanistic analysis showed that appropriate electrical stimulation could upregulate calcium ion concentration while inhibit the activation of SOCE and inflammation-related signaling pathways. However, over-voltage stimulation increased ROS levels and reactivated pro-inflammatory signaling pathways. In general, benefiting from having both collagen biochemical cues and the ability to regulate the electrical microenvironment, CPF enabled astrocytes to have the lowest inflammatory factor secretion and inflammatory marker expression under appropriate electrical stimulation, effectively inhibiting the exacerbation of neuroinflammation. This work provides a new perspective on anti-neuroinflammation of the electrode interfaces.
与植入神经电极界面上星形胶质细胞的炎性激活相关的神经炎症是电极失效的主要原因。在这项工作中，设计并制备了胶原蛋白/聚吡咯复合膜（CPF）来修饰该界面。CPF在形态上具有胶原蛋白和聚吡咯的共同暴露，这使得胶原蛋白提供的仿生微环境能够有效抑制星形胶质细胞的炎性激活。同时，复合膜中的聚吡咯显著改善了电极界面的电化学性能，使其能够提供一种在电刺激下抑制星形胶质细胞炎性激活的电微环境。此外，机制分析表明，适当的电刺激可以上调钙离子浓度，同时抑制SOCE和炎症相关信号通路的激活。然而，过电压刺激会增加ROS水平并重新激活促炎信号通路。总体而言，得益于具有胶原蛋白生化线索和调节电微环境的能力，CPF使得星形胶质细胞在适当的电刺激下具有最低的炎症因子分泌和炎症标志物表达，有效抑制了神经炎症的加剧。这项工作为电极界面的抗神经炎症提供了新的视角。
