珍宝丸通过miR-214-5p/SOX4/β-catenin轴抑制小胶质细胞激活以改善脊髓损伤

Journal of physiological investigation Pub Date : 2024-09-01 Epub Date: 2024-10-28 DOI:10.4103/ejpi.EJPI-D-23-00025
Yanqiang Huan, Juan He, Pengfei Li, Fei Wang, Huidong Zhou, Yongxiong He
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引用次数: 0

摘要

摘要:研究表明,珍宝丸(ZBP)可改善脊髓损伤(SCI)的预后。然而,其在 SCI 中的潜在调控机制仍有待阐明。本研究的目的是在体外和体内明确 ZBP 在 SCI 中的作用及其潜在的分子机制。我们的研究结果表明,ZBP 在体内通过增强 miR-214-5p 抑制神经元凋亡和炎症反应,从而改善 SCI。在体外,ZBP 通过 miR-214-5p 显著降低了氧-葡萄糖剥夺(OGD)激活的小胶质细胞诱导的炎症因子水平、提高了细胞活力并减少了细胞凋亡。此外,添加 miR-214-5p 还能减轻 OGD 处理的小胶质细胞的炎症反应、提高细胞活力并抑制细胞凋亡。我们发现 SRY-box 转录因子 4(SOX4)是 miR-214-5p 的潜在靶点。过表达 SOX4 可抵消 miR-214-5p 对 OGD 激活的小胶质细胞的炎症反应、细胞活力和细胞凋亡的影响。ZBP 通过增强活化小胶质细胞中的 miR-214-5p 抑制了 SOX4/β-catenin 的活化并减少了促炎细胞因子的分泌。总之,我们的研究结果表明,ZBP 可通过 miR-214-5p/SOX4/β-catenin 轴抑制活化小胶质细胞造成的神经元损伤,从而缓解 SCI,为 ZBP 作为 SCI 治疗药物的分子基础提供了宝贵的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Zhenbao Pill Attenuates Microglia Activation to Improve Spinal Cord Injury via miR-214-5p/SOX4/β-catenin Axis.

Abstract: Zhenbao pill (ZBP) has been shown to improve outcomes in spinal cord injury (SCI). However, its potential regulatory mechanisms in SCI remain to be elucidated. This study aimed to define the role of ZBP and its underlying molecular mechanisms in SCI, both in vitro and in vivo. Our findings indicated that ZBP ameliorated SCI by inhibiting neuronal apoptosis and the inflammatory response through the enhancement of miR-214-5p in vivo. In vitro, ZBP significantly reduced the levels of inflammatory factors, increased cell viability, and decreased apoptosis induced by oxygen-glucose deprivation (OGD)-activated microglia via miR-214-5p. Furthermore, the addition of miR-214-5p diminished the inflammatory response, enhanced cell viability, and suppressed apoptosis in OGD-treated microglia. We identified SRY-box transcription factor 4 (SOX4) as a potential target of miR-214-5p. Overexpression of SOX4 negated the effects of miR-214-5p on the inflammatory response, cell viability, and apoptosis in OGD-activated microglia. ZBP inhibited SOX4/β-catenin activation and reduced pro-inflammatory cytokine secretion by enhancing miR-214-5p in activated microglia. In summary, our findings demonstrate that ZBP mitigates SCI by inhibiting neuronal damage caused by activated microglia through the miR-214-5p/SOX4/β-catenin axis, providing valuable insights into the molecular basis of ZBP as a therapeutic agent for SCI.

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