PMID- 28687236
OWN - NLM
STAT- MEDLINE
DCOM- 20180101
LR  - 20191210
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Linking)
VI  - 655
DP  - 2017 Aug 10
TI  - Sevoflurane suppresses microglial M2 polarization.
PG  - 160-165
LID - S0304-3940(17)30552-9 [pii]
LID - 10.1016/j.neulet.2017.07.001 [doi]
AB  - Microglia can be polarized into the classical (M1) or alternative (M2) activation 
      states in response to various stimuli. The M2 phenotype has its own set of 
      receptor profiles, cytokine production, and chemokine secretion, of which 
      arginase 1 (Arg1), chitinase 3-like 3 (Chi3l3, Ym1), and IL-10 have 
      neuroprotective properties. Sevoflurane is one of the most commonly used volatile 
      anesthetics in clinics. Previous studies have shown that sevoflurane promotes 
      microglial M1 activation. However, it remains unclear whether sevoflurane 
      regulates microglial M2 activation. In this study, we found that sevoflurane 
      treatment abolished interleukin 4 (IL-4)-induced M2 microglial activation. Our 
      results indicate that IL-4-mediated induction of the characteristic M2 marker 
      genes and proteins Arg1, Ym1, and IL-10 was significantly attenuated by 
      sevoflurane pretreatment in primary microglia. Microglial M2 polarization induced 
      by incubation with culture supernatant from human umbilical cord mesenchymal 
      stromal cells (HUC-MSCs) was abolished by treatment with 2% or 4% sevoflurane. 
      Upregulation of SOCS1 and suppression of SOCS3 were shown to play a crucial role 
      in the process of M2 microglial polarization. Our results also indicate that 
      SOCS1 expression was induced by IL-4, but it was inhibited by pretreatment with 
      sevoflurane. In contrast, IL-4 suppressed SOCS3 expression, which was restored by 
      pretreatment with sevoflurane. Mechanistically, it was shown that sevoflurane 
      suppresses STAT6 phosphorylation in primary microglia.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Pei, Zengyang
AU  - Pei Z
AD  - Department of Veterinary Medicine, College of Animal Sciences, Zhejiang 
      University, 866 Yuhangtang Road, Hangzhou 310058, PR China. Electronic address: 
      kywang82@163.com.
FAU - Wang, Shenghao
AU  - Wang S
AD  - Department of Veterinary Medicine, College of Animal Sciences, Zhejiang 
      University, 866 Yuhangtang Road, Hangzhou 310058, PR China.
FAU - Li, Qi
AU  - Li Q
AD  - Department of Veterinary Medicine, College of Animal Sciences, Zhejiang 
      University, 866 Yuhangtang Road, Hangzhou 310058, PR China.
LA  - eng
PT  - Journal Article
DEP - 20170704
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Anesthetics, Inhalation)
RN  - 0 (Lectins)
RN  - 0 (Methyl Ethers)
RN  - 0 (Socs3 protein, mouse)
RN  - 0 (Suppressor of Cytokine Signaling 3 Protein)
RN  - 130068-27-8 (Interleukin-10)
RN  - 38LVP0K73A (Sevoflurane)
RN  - EC 3.2.1.52 (Chil3 protein, mouse)
RN  - EC 3.2.1.52 (beta-N-Acetylhexosaminidases)
RN  - EC 3.5.3.1 (Arg1 protein, mouse)
RN  - EC 3.5.3.1 (Arginase)
SB  - IM
MH  - Anesthetics, Inhalation/*pharmacology
MH  - Animals
MH  - Arginase/metabolism
MH  - Cell Polarity
MH  - Cells, Cultured
MH  - Interleukin-10/metabolism
MH  - Lectins/metabolism
MH  - Methyl Ethers/*pharmacology
MH  - Mice
MH  - Microglia/*drug effects/physiology
MH  - Sevoflurane
MH  - Suppressor of Cytokine Signaling 3 Protein/metabolism
MH  - beta-N-Acetylhexosaminidases/metabolism
OTO - NOTNLM
OT  - M2 polarization
OT  - Microglia
OT  - STAT6
OT  - Sevoflurane
EDAT- 2017/07/09 06:00
MHDA- 2018/01/02 06:00
CRDT- 2017/07/09 06:00
PHST- 2016/12/09 00:00 [received]
PHST- 2017/06/30 00:00 [revised]
PHST- 2017/07/03 00:00 [accepted]
PHST- 2017/07/09 06:00 [pubmed]
PHST- 2018/01/02 06:00 [medline]
PHST- 2017/07/09 06:00 [entrez]
AID - S0304-3940(17)30552-9 [pii]
AID - 10.1016/j.neulet.2017.07.001 [doi]
PST - ppublish
SO  - Neurosci Lett. 2017 Aug 10;655:160-165. doi: 10.1016/j.neulet.2017.07.001. Epub 
      2017 Jul 4.