PMID- 34223957
OWN - NLM
STAT- MEDLINE
DCOM- 20210921
LR  - 20210921
IS  - 1432-1106 (Electronic)
IS  - 0014-4819 (Linking)
VI  - 239
IP  - 9
DP  - 2021 Sep
TI  - Neuroprotection of sevoflurane against ischemia/reperfusion-induced brain injury 
      through inhibiting GluN2A/GluN2B-PSD-95-MLK3 module.
PG  - 2701-2709
LID - 10.1007/s00221-021-06157-x [doi]
AB  - To investigate the role of GluN2A and GluN2B in neuroprotective effect of 
      sevoflurane preconditioning against cerebral ischemia-reperfusion injury (CIRI). 
      Rats were randomly divided into five groups as follows: control, 
      ischemia-reperfusion (I/R) 6 h, sevoflurane preconditioning (SP), 
      SP + amantadine, SP + NMDA. Immunoblot and immunoprecipitation were used to 
      detect the tyrosine phosphorylation of GluN2A/GluN2B, the interaction of 
      GluN2A/GluN2B-PSD-95-MLK3 and the expression of phosphorylation of MLK3, MKK7 and 
      JNK3. Cresyl violet staining was employed to analyse neuronal injury in rat 
      hippocampal CA1 subfields. Sevoflurane preconditioning inhibits the tyrosine 
      phosphorylation of GluN2A/GluN2B, the interaction of GluN2A/GluN2B-PSD-95-MLK3 
      and the phosphorylation of MLK3, MKK7 and JNK3 in rat hippocampus. An 
      N-methyl-D-aspartate receptor (NMDAR) antagonist amantadine reversed the 
      MLK3-MKK7- JNK3 signal events. Such reversion was also realized by NMDA (60 and 
      80 nmol) and low doses of NMDA (0-40 nmol) could not change the inhibitory effect 
      of sevoflurane preconditioning on MLK3-MKK7-JNK3 signal events. Finally, Cresyl 
      violet staining also confirmed that low dose of NMDA reduced neuronal loss in rat 
      hippocampal CA1 subfields. Sevoflurane preconditioning provides neuroprotection 
      against CIRI by inhibiting NMDAR over-activation.
CI  - (c) 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
      part of Springer Nature.
FAU - Jin, Lei
AU  - Jin L
AD  - Medical Biological Experiment Credit Center, Basic Medical College, Xuzhou 
      Medical University, Xuzhou, Jiangsu, China. jinlei@xzhmu.edu.cn.
FAU - Bo, Xiu Mei
AU  - Bo XM
AD  - Medical Biological Experiment Credit Center, Basic Medical College, Xuzhou 
      Medical University, Xuzhou, Jiangsu, China.
LA  - eng
PT  - Journal Article
DEP - 20210705
PL  - Germany
TA  - Exp Brain Res
JT  - Experimental brain research
JID - 0043312
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 38LVP0K73A (Sevoflurane)
RN  - EC 2.7.11.25 (MAP Kinase Kinase Kinases)
SB  - IM
MH  - Animals
MH  - *Brain Injuries
MH  - MAP Kinase Kinase Kinases/metabolism
MH  - Neuroprotection
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, N-Methyl-D-Aspartate
MH  - Reperfusion
MH  - *Reperfusion Injury/drug therapy
MH  - Sevoflurane
OTO - NOTNLM
OT  - CIRI
OT  - GluN2A
OT  - GluN2B
OT  - MLK3
OT  - PSD-95
OT  - Sevoflurane
EDAT- 2021/07/06 06:00
MHDA- 2021/09/22 06:00
CRDT- 2021/07/05 12:20
PHST- 2021/02/16 00:00 [received]
PHST- 2021/06/19 00:00 [accepted]
PHST- 2021/07/06 06:00 [pubmed]
PHST- 2021/09/22 06:00 [medline]
PHST- 2021/07/05 12:20 [entrez]
AID - 10.1007/s00221-021-06157-x [pii]
AID - 10.1007/s00221-021-06157-x [doi]
PST - ppublish
SO  - Exp Brain Res. 2021 Sep;239(9):2701-2709. doi: 10.1007/s00221-021-06157-x. Epub 
      2021 Jul 5.