PMID- 31853322
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 19
IP  - 1
DP  - 2020 Jan
TI  - miR-9 inhibition of neuronal apoptosis and expression levels of apoptosis genes 
      Bcl-2 and Bax in depression model rats through Notch pathway.
PG  - 551-556
LID - 10.3892/etm.2019.8228 [doi]
AB  - Effects of micro ribonucleic acid (miR)-9 on neuronal apoptosis and expression 
      levels of apoptosis genes B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X 
      protein (Bax) in depression model rats, as well as its regulatory mechanism, were 
      investigated. Thirty Sprague-Dawley rats were randomly divided into control group 
      (n=10), model group (n=10) and miR-9 inhibitor group (n=10). The rat model of 
      depression was established using the chronic stress method. The learning and 
      memory abilities of rats were detected via water maze test, the neuronal 
      morphology of the brain was detected using hematoxylin and eosin (H&E) staining, 
      and the levels of serum Bcl-2 and Bax were determined using the enzyme-linked 
      immunosorbent assay (ELISA) kits. Moreover, the neuronal apoptosis in the brain 
      was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick 
      end labeling (TUNEL) assay, and the protein levels of Notch1 and Hes1 in brain 
      tissues were measured via western blot analysis. Compared with the control group, 
      the rats in the model group presented significantly decreased learning and memory 
      abilities, poor neuronal morphology of the brain, significantly higher neuronal 
      apoptosis rate in the brain, decreased level of serum Bcl-2, increased level of 
      serum Bax, and significantly decreased protein levels of Notch1 and Hes1 in brain 
      tissues. Compared with the model group, the rats in miR-9 inhibitor group showed 
      obviously improved learning and memory abilities, improved neuronal morphology of 
      the brain, an obviously lower neuronal apoptosis rate in the brain, increased 
      level of serum Bcl-2, decreased level of serum Bax, and obviously increased 
      protein levels of Notch1 and Hes1 in brain tissues. In conclusion, miR-9 
      inhibitor can promote the neurological function recovery and inhibit the neuronal 
      apoptosis of depression model rats through activating the Notch signaling 
      pathway, suggesting that miR-9 can be an important therapeutic target for 
      depression.
CI  - Copyright: (c) Xiao et al.
FAU - Xiao, Peng
AU  - Xiao P
AD  - Department of Psychiatry, Jining Psychiatric Hospital, Jining, Shandong 272051, 
      P.R. China.
FAU - Zhang, Xiaoming
AU  - Zhang X
AD  - Department of Psychiatry, Jining Psychiatric Hospital, Jining, Shandong 272051, 
      P.R. China.
FAU - Li, Yanfei
AU  - Li Y
AD  - Department of Psychiatry, Jining Psychiatric Hospital, Jining, Shandong 272051, 
      P.R. China.
FAU - Ma, Zhongyi
AU  - Ma Z
AD  - Department of Psychiatry, Jining Psychiatric Hospital, Jining, Shandong 272051, 
      P.R. China.
FAU - Si, Shuping
AU  - Si S
AD  - Department of Psychiatry, Jining Psychiatric Hospital, Jining, Shandong 272051, 
      P.R. China.
FAU - Gao, Xinxue
AU  - Gao X
AD  - Department of Psychiatry, Jining Psychiatric Hospital, Jining, Shandong 272051, 
      P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20191121
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC6909800
OTO - NOTNLM
OT  - Notch signaling pathway
OT  - apoptosis
OT  - depression
OT  - miR-9
OT  - neurons
EDAT- 2019/12/20 06:00
MHDA- 2019/12/20 06:01
PMCR- 2019/11/21
CRDT- 2019/12/20 06:00
PHST- 2019/09/09 00:00 [received]
PHST- 2019/11/06 00:00 [accepted]
PHST- 2019/12/20 06:00 [entrez]
PHST- 2019/12/20 06:00 [pubmed]
PHST- 2019/12/20 06:01 [medline]
PHST- 2019/11/21 00:00 [pmc-release]
AID - ETM-0-0-8228 [pii]
AID - 10.3892/etm.2019.8228 [doi]
PST - ppublish
SO  - Exp Ther Med. 2020 Jan;19(1):551-556. doi: 10.3892/etm.2019.8228. Epub 2019 Nov 
      21.