ORIGINAL RESEARCH article
Front. Psychiatry
Sec. Autism
Volume 16 - 2025 | doi: 10.3389/fpsyt.2025.1630782
Plasma exosomal miR-30b-5p attenuates neuroinflammation in a rat model of autism spectrum disorder
Provisionally accepted
- The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
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There is growing evidence that exosomes play an important role in the pathogenesis of central nervous system diseases, but little is known about the relationship between exosomes and autism spectrum disorder (ASD). In this study, a rat model of ASD was generated via prenatal exposure to valproic acid (VPA). VPA-exposed rats exhibited ASD-like behaviors. The plasma exosomal microRNA (miRNA) expression profiles of VPA-treated rats and sham rats were analyzed. We found that the level of miR-30b-5p was significantly lower in the plasma exosomes and brains of VPA-exposed rats than in those of sham rats. In addition, the levels of inflammatory factors, epidermal growth factor receptor (EGFR), p-p38/p38, and CaMKII were increased in the brains of VPA-exposed rats. Moreover, overexpressing miR-30b-5p ameliorates ASD-like behaviors and decreases the expression of inflammatory factors, EGFR, p-p38/p38, and CaMKII in the brains of VPA-exposed rats. In conclusion, our study highlights that plasma exosomal miR-30b-5p attenuates neuroinflammation in a rat model of ASD by modulating EGFR through the MAPK signaling pathway and calcium signaling pathway. This study provides novel perspectives on plasma exosomal miR-30b-5p, which could be considered a potential therapeutic target for the treatment of ASD in the clinic.
Keywords: Exosomes, Autism Spectrum Disorder, miR-30b-5p, EGFR, Neuroinflammation
Received: 18 May 2025; Accepted: 19 Sep 2025.
Copyright: © 2025 Zheng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Zhen Zheng, zhengzhen0320@126.com
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