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Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
Published on: December 8, 2017
Alleviation of neuroinflammation on electrode interface by biomimetic electrical microenvironment modulation based on
Chengwei Wu1, Xiyue Duan1, Xuzhao He1
1Department 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.
Abstract:
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.

