Oxidized sodium alginate hydrogel-mouse nerve growth factor sustained release system promotes repair of peripheral nerve injury

神经生长因子 周围神经损伤 药理学 坐骨神经 体内 神经损伤 生长因子 MAPK/ERK通路 化学 激酶 医学 内科学 生物 麻醉 受体 生物化学 生物技术
作者
Yu-ming Sun,Xiangyu Sun,Ruiqi Wang,Yuhang Xing,Xiang Ma,Jie Yue,Min Zhang,Yuezhu Wang,Weiming Tian,Guangping Jing,Yu-ming Sun,Xiangyu Sun,Ruiqi Wang,Yuhang Xing,Xiang Ma,Jie Yue,Min Zhang,Yuezhu Wang,Weiming Tian,Guangping Jing
出处
期刊:Journal of Biomaterials Science-polymer Edition [Informa]
卷期号:35 (10): 1550-1570 被引量:5
标识
DOI:10.1080/09205063.2024.2339636
摘要

In recent years, mouse nerve growth factor (mNGF) has emerged as an important biological regulator to repair peripheral nerve injury, but its systemic application is restricted by low efficiency and large dosage requirement. These limitations prompted us to search for biomaterials that can be locally loaded. Oxidized sodium alginate hydrogel (OSA) exhibits good biocompatibility and physicochemical properties, and can be loaded with drugs to construct a sustained-release system that can act locally on nerve injury. Here, we constructed a sustained-release system of OSA-mouse nerve growth factor (mNGF), and investigated the loading and release of the drug through Fourier transform infrared spectroscopy and drug release curves. In vitro and in vivo experiments showed that OSA-mNGF significantly promoted the biological activities of RSC-96 cells and facilitated the recovery from sciatic nerve crush injury in rats. This observation may be attributed to the additive effect of OSA on promoting Schwann cell biological activities or its synergistic effect of cross-activating phosphoinositide 3-kinase (PI3K) through extracellular signal regulated kinase (ERK) signaling. Although the specific mechanism of OSA action needs to be explored in the future, the current results provide a valuable preliminary research basis for the clinical application of the OSA-mNGF sustained-release system for nerve repair.
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