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

Abstract:

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 α (TNF-α), and interleukin-1β (IL-1β) 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-α and IL-1β 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.

journal_name

Int Immunopharmacol

authors

Guo H,Huang B,Wang Y,Zhang Y,Ma Q,Ren Y

doi

10.1016/j.intimp.2020.106285

subject

Has Abstract

pub_date

2020-02-20 00:00:00

pages

106285

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(19)32318-5

journal_volume

82

pub_type

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