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

NeuroReport

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Cellular, Molecular and Developmental Neuroscience

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

Author Information

Department of Neurology, Qilu Hospital of Shandong University, Jinan, China

Received 2 November 2023 Accepted 15 April 2024.

Correspondence to Xiuhe Zhao, PhD, Department of Neurology, Qilu Hospital of Shandong University, No.107 West Wenhua Road, Jinan, Shandong Province 250012, China Tel: +0531 82169351; e-mail: [email protected]

NeuroReport | DOI: 10.1097/WNR.0000000000002044 Metrics

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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