The miR-23b-3p from adipose-derived stem cell exosomes alleviate inflammation in mice experiencing kainic acid-induced epileptic seizures.

IF 1.6 4区医学 Q4 NEUROSCIENCES

Neuroreport Pub Date : 2024-07-01 Epub Date: 2024-05-09 DOI:10.1097/WNR.0000000000002044

Xue Yang, Xiaxin Yang, Anqi Sun, Si Chen, Xiaotang Wang, Xiuhe Zhao

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Abstract

Epilepsy is a common neurologic disorder. While a good clinical solution is still missing, studies have confirmed that exosomes (Exos) derived from adipose-derived stem cells (ADSCs) had a therapeutic effect on various diseases, including neurological diseases. Therefore, this study aimed to reveal whether ADSC-Exo treatment could improve kainic acid (KA)-induced seizures in epileptic mice. ADSCs and Exos were isolated. Mice were generated with KA-induced epileptic seizures. ELISA was used to detect inflammatory factor expression. Luciferase reporter analysis detection showed a relationship among miR-23b-3p, STAT1, and glyoxylate reductase 1 (GlyR1). ADSC-Exos had a protective effect on KA-induced seizures by inhibiting inflammatory factor expression and the M1 microglia phenotype. The result showed that miR-23b-3p played an important role in the Exo-mediated protective effect in KA-induced seizures in epileptic mice by regulating STAT1 and GlyR1. Luciferase reporter analysis confirmed that miR-23b-3p interacted with the 3'-UTR of STAT1 and GlyR1. The miR-23b-3p inhibited M1 microglia-mediated inflammatory factor expression in microglial cells by regulating STAT1 and GlyR1. The downregulation of miR-23b-3p decreased the protective effect of ADSC-Exos on KA-induced seizures in epileptic mice. The miR-23b-3p from ADSC-Exos alleviated inflammation in mice with KA-induced epileptic seizures.

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脂肪源性干细胞外泌体中的 miR-23b-3p 可减轻凯尼酸诱发的癫痫小鼠的炎症反应。

癫痫是一种常见的神经系统疾病。虽然目前还没有很好的临床解决方案，但已有研究证实，从脂肪源性干细胞（ADSCs）中提取的外泌体（Exos）对包括神经系统疾病在内的多种疾病有治疗作用。因此，本研究旨在揭示ADSC-Exo治疗是否能改善凯尼酸（KA）诱导的癫痫小鼠癫痫发作。研究分离了 ADSCs 和 Exos。生成 KA 诱导癫痫发作的小鼠。用ELISA检测炎症因子的表达。荧光素酶报告分析检测显示了 miR-23b-3p、STAT1 和乙醛酸还原酶 1 (GlyR1) 之间的关系。ADSC-Exos 通过抑制炎症因子的表达和 M1 小胶质细胞表型，对 KA 诱导的癫痫发作有保护作用。研究结果表明，miR-23b-3p通过调节STAT1和GlyR1，在Exo介导的对KA诱导的癫痫小鼠发作的保护作用中发挥了重要作用。荧光素酶报告分析证实，miR-23b-3p 与 STAT1 和 GlyR1 的 3'-UTR 相互作用。miR-23b-3p 通过调节 STAT1 和 GlyR1 抑制了 M1 小胶质细胞介导的小胶质细胞炎症因子的表达。miR-23b-3p 的下调降低了 ADSC-Exos 对 KA 诱导的癫痫小鼠癫痫发作的保护作用。来自 ADSC-Exos 的 miR-23b-3p 减轻了 KA 诱导的癫痫小鼠的炎症反应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroreport 医学-神经科学

CiteScore

3.20

自引率

0.00%

发文量

150

审稿时长

1 months

期刊介绍： NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.