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GDNF-凝胶/HA-Mg神经导管的制备及其在修复周围神经缺损中的作用。

Fabrication of GDNF-Gel/HA-Mg nerve conduit and its role in repairing peripheral nerve defects.

作者信息

Cai Yuanqing, Chen Yi, Li Hongyan, Wang Yanyu, Zhang Guangyang, Liang Jialin, Lv Leifeng, Huang Ying, Zhang Wenming, Dang Xiaoqian, Fang Xinyu, Wang Yong

机构信息

Department of Orthopaedic Surgery, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.

College of Materials Science & Engineering, National Engineering Research Center for Magnesium Alloys, Chongqing University, Chongqing, 400045, China.

出版信息

Mater Today Bio. 2025 Apr 12;32:101764. doi: 10.1016/j.mtbio.2025.101764. eCollection 2025 Jun.

DOI:10.1016/j.mtbio.2025.101764
PMID:40290886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12022700/
Abstract

BACKGROUND

Magnesium (Mg) and its alloys are receiving increasing attention in peripheral nerve regeneration, but they were limited due to the low corrosion resistance and rapid degradation. In this study, GDNF-Gel/HA-Mg was prepared and its value in peripheral nerve defects repairment was explored both and .

METHODS

A hydroxyapatite (HA) coating was first applied to the pure Mg surface, followed by the formation of gelatin methacrylate (GelMA) loaded with glial cell-derived neurotrophic factor (GDNF) on the HA-coated Mg surface. GDNF-Gel/HA-Mg corrosion resistance was explored. The effect of GDNF-Gel/HA-Mg conduit on Schwann cell proliferation and migration abilities were investigated. And sciatic nerve defects models were established to explored the role of GDNF-Gel/HA-Mg conduit in peripheral nerve defects repairment.

FINDINGS

The electrochemical, immersion, and hydrogen evolution experiments indicated that the corrosion resistance in phosphate buffer saline (PBS) of pure Mg was significantly improved by the GDNF-Gel/HA coating. Cell cycle, Cell Count Kit-8 (CCK-8), and clone formation assays indicated that GDNF-Gel/HA-Mg promoted the proliferation of Schwann cells. Scratch and Transwell assay results demonstrated that GDNF-Gel/HA-Mg promoted Schwann cell migration ability dose-dependently. GDNF-Gel/HA-Mg was found to enhance the secretion of nerve growth factor (NGF) and the expression of p75. Flow cytometry results showed that GDNF-Gel/HA-Mg could reduce HO-induced oxidative stress and Schwann cell apoptosis. GDNF-Gel/HA-Mg inhibited M1 macrophage polarization while facilitated M2 macrophage polarization in a concentration-dependent manner. The studies demonstrated that GDNF-Gel/HA-Mg conduit could significantly promote the regeneration and myelination of sciatic nerve, as well as the recovery of denervated gastrocnemius atrophy.

INTERPRETATION

The GDNF-Gel/HA-Mg conduit prepared in this study exhibited good hydrophilicity and corrosion resistance and greatly enhanced the proliferation, migration, and invasion abilities of Schwann cells, as well as peripheral nerve regeneration.

摘要

背景

镁（Mg）及其合金在周围神经再生中受到越来越多的关注，但由于其耐腐蚀性低和降解迅速而受到限制。在本研究中，制备了GDNF-Gel/HA-Mg，并从体内和体外两方面探讨了其在周围神经缺损修复中的价值。

方法

首先在纯镁表面涂覆羟基磷灰石（HA）涂层，然后在HA涂层的镁表面形成负载胶质细胞源性神经营养因子（GDNF）的甲基丙烯酸明胶（GelMA）。研究了GDNF-Gel/HA-Mg的耐腐蚀性。研究了GDNF-Gel/HA-Mg导管对雪旺细胞增殖和迁移能力的影响。建立坐骨神经缺损模型，探讨GDNF-Gel/HA-Mg导管在周围神经缺损修复中的作用。

结果

电化学、浸泡和析氢实验表明，GDNF-Gel/HA涂层显著提高了纯镁在磷酸盐缓冲盐水（PBS）中的耐腐蚀性。细胞周期、细胞计数试剂盒-8（CCK-8）和克隆形成试验表明，GDNF-Gel/HA-Mg促进了雪旺细胞的增殖。划痕试验和Transwell试验结果表明，GDNF-Gel/HA-Mg剂量依赖性地促进雪旺细胞迁移能力。发现GDNF-Gel/HA-Mg可增强神经生长因子（NGF）的分泌和p75的表达。流式细胞术结果表明，GDNF-Gel/HA-Mg可降低过氧化氢（HO）诱导的氧化应激和雪旺细胞凋亡。GDNF-Gel/HA-Mg抑制M1巨噬细胞极化，同时以浓度依赖的方式促进M2巨噬细胞极化。体内研究表明，GDNF-Gel/HA-Mg导管可显著促进坐骨神经的再生和髓鞘形成，以及失神经支配的腓肠肌萎缩的恢复。

结论

本研究制备的GDNF-Gel/HA-Mg导管具有良好的亲水性和耐腐蚀性，大大增强了雪旺细胞的增殖、迁移和侵袭能力，以及周围神经再生能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/cf4de01288e2/mmcfigs3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/8fd940efd216/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/79d119649220/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/037834ce8329/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/f4796cc1f69d/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/3e72254e34a6/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/5d3a52f5d85a/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/29f7906a4baa/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/ec10dc49ca47/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/3688f11dd6e0/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/f79968da4e2e/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/0df3b20cd370/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/466e49720ad0/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/4502e5c7a41c/mmcfigs1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6af5/12022700/cf4de01288e2/mmcfigs3.jpg

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