4.7 Article

Bone marrow mesenchymal stem cells-derived exosomes improve injury of hippocampal neurons in rats with depression by upregulating microRNA-26a expression

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INTERNATIONAL IMMUNOPHARMACOLOGY
卷 82, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.intimp.2020.106285

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Bone marrow mesenchymal stem cells; Exosomes; MicroRNA-26a; Depression; Hippocampal neurons

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Objective: Bone marrow mesenchymal stem cells (BMSCs)-derived exosomes have been widely applied in disease therapies. However, the role of BMSCs-derived exosomes in depression remains obscure. This study aims to explore the mechanism of BMSCs-derived exosomal microRNA-26a (miR-26a) on hippocampal neuronal injury of depressed rats. Methods: BMSCs and their exosomes were obtained and identified. Rat models of depression were established by corticosterone injection, then injected with BMSCs-derived exosomes. The contents of superoxide dismutase (SOD), imalondialdehyde (MDA), lactate dehydrogenase (LDH), tumor necrosis factor alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta) in rats' serum, hippocampal tissues and neurons were determined. The expression of miR-26a in hippocampal tissues and neurons was detected by RT-qPCR. The injury models of rat hippocampal neurons were established to figure out the role of BMSCs-derived exosomes and miR-26a in neuron apoptosis and proliferation. Results: In hippocampal tissues of depressed rats, miR-26a was lowly expressed, and BMSCs-derived exosomes upregulated miR-26a expression. BMSCs-derived exosomes restrained apoptosis in hippocampal tissues of depressed rats. BMSCs-derived exosomes and upregulated miR-26a elevated SOD level, lessened MDA, LDH, TNF-alpha and IL-1 beta levels, boosted hippocampal neuron proliferation and suppressed apoptosis in depressed rats. Conclusion: Collectively, our study reveals that miR-26a is lowly expressed in depressed rats, and BMSCs-derived exosomes improve hippocampal neuron injury of rat with depression by upregulating miR-26a.

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