Bone marrow mesenchymal stem cells-derived exosomes improve injury of hippocampal neurons in rats with depression by upregulating microRNA-26a expression.
Int Immunopharmacol
; 82: 106285, 2020 Feb 20.
Article
in En
| MEDLINE
| ID: mdl-32088640
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-1ß (IL-1ß) 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-1ß 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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Type of study:
Prognostic_studies
Language:
En
Journal:
Int Immunopharmacol
Journal subject:
ALERGIA E IMUNOLOGIA
/
FARMACOLOGIA
Year:
2020
Document type:
Article