miR-381-3p protects hippocampal neurons of depressive rats from injury via BDNF
10.3969/j.issn.1000-4718.2018.04.019
- VernacularTitle:miR-381-3p通过BDNF减轻抑郁症大鼠海马区细胞损伤
- Author:
Na LEI
1
;
Xue-Ping ZHANG
;
Chuang WANG
Author Information
1. 杭州市第七人民医院精神科
- Keywords:
Depression;
MicroRNA-381-3p;
Brain-derived neurotrophic factor;
Hippocampal neurons
- From:Chinese Journal of Pathophysiology
2018;34(4):699-704
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of microRNA(miR)-381-3p on neuronal injury in the hippocampus of depressive rats and the possible regulatory mechanism.METHODS:The rat model of depression was established by sub-cutaneous injection of corticosterone and the model rats received fluoxetine treatment.The body weight,open field test and biochemical indexes were measured for judging the therapeutic effect of fluoxetine.The expression of miR-381-3p,brain-derived neurotrophic factor(BNDF),Bcl-2 and Bax in the hippocampus was determined.The cultured neonatal rat hipp-ocampal neurons were pre-transfected with miR-381-3p inhibitor and then incubated with corticosterone.The cell viability, and the expression of miR-381-3p, BNDF, Bcl-2 and Bax were detected.The targeted regulatory role of miR-381-3p in BDNF was verified by luciferase reporter assay.RESULTS:Compared with depression group,fluoxetine increased the body weight,the number of cross-field activities and the content of norepinephrine,inhibited the expression of miR-381-3p and promoted the expression of BNDF in the hippocampus.miR-381-3p silencing reversed the effect of corticosterone,resulting in the increase in the survival rate of hippocampal neurons, upregulation of BDNF and Bcl-2, and downregulation of Bax expression.miR-381-3p targeted the regulation of BNDF expression.CONCLUSION: Silencing miR-381-3p protects rat hippocampal neurons from corticosterone injury,and its mechanism may be related to the upregulation of BNDF expression.
