PMID- 26257854
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150810
LR  - 20181113
IS  - 2005-6419 (Print)
IS  - 2005-7563 (Electronic)
IS  - 2005-6419 (Linking)
VI  - 68
IP  - 4
DP  - 2015 Aug
TI  - Therapeutic effects of intravenous administration of bone marrow stromal cells on 
      sevoflurane-induced neuronal apoptosis and neuroinflammation in neonatal rats.
PG  - 397-401
LID - 10.4097/kjae.2015.68.4.397 [doi]
AB  - BACKGROUND: Sevoflurane exposure during the early postnatal period causes 
      neuroinflammation and neuronal apoptosis in rodents. Bone marrow stromal cells 
      (BMSCs) have been shown to protect and repair the damaged central nervous system, 
      for example in ischemic stroke models. In this study, we investigated whether 
      intravenous administration of BMSCs ameliorated neurodegeneration, induced by 
      sevoflurane exposure, in neonatal rats. METHODS: Sprague-Dawley rat pups 
      (postnatal day 7) were exposed to 2% sevoflurane for 6 h (vehicle group, n = 7). 
      BMSCs were administered 30 min after induction of sevoflurane anesthesia (BMSCs 
      group, n = 7). The pups were exposed to carrier gas only, as a negative control 
      (mock anesthesia group, n = 4). We assessed the therapeutic effects of BMSC 
      treatment by measuring expression of the pro-inflammatory cytokine interleukin-6 
      (IL-6), and levels of cleaved caspase-3, in brain tissues immediately following 
      sevoflurane anesthesia. RESULTS: Analysis of the cleaved caspase-3 bands revealed 
      that levels of activated caspase-3 were elevated in the vehicle group compared 
      with the mock anesthesia group, indicating that a single exposure to sevoflurane 
      at subclinical concentrations can precipitate neuronal apoptosis. BMSC treatment 
      did not suppress apoptosis induced by sevoflurane exposure (compared with the 
      vehicle group). The vehicle group had higher proinflammatory cytokine IL-6 
      protein levels compared with the mock anesthesia group, indicating that 
      sevoflurane exposure induces IL-6 expression. BMSC treatment suppressed 
      sevoflurane-induced increases in IL-6 expression, indicating that these cells can 
      inhibit the neuroinflammation induced by sevoflurane exposure (vehicle group vs. 
      BMSC group). CONCLUSIONS: Intravenous administration of BMSCs reduces 
      neuroinflammation, but does not attenuate apoptosis induced by sevoflurane 
      exposure.
FAU - Sun, ZhongLiang
AU  - Sun Z
AD  - Department of Anesthesiology, Graduate School of Medical and Dental Sciences, 
      Tokyo Medical and Dental University, Tokyo, Japan.
FAU - Satomoto, Maiko
AU  - Satomoto M
AD  - Department of Anesthesiology, Graduate School of Medical and Dental Sciences, 
      Tokyo Medical and Dental University, Tokyo, Japan.
FAU - Makita, Koshi
AU  - Makita K
AD  - Department of Anesthesiology, Graduate School of Medical and Dental Sciences, 
      Tokyo Medical and Dental University, Tokyo, Japan.
LA  - eng
PT  - Journal Article
DEP - 20150728
PL  - Korea (South)
TA  - Korean J Anesthesiol
JT  - Korean journal of anesthesiology
JID - 101502451
PMC - PMC4524940
OTO - NOTNLM
OT  - Apoptosis
OT  - Bone marrow stromal cells
OT  - Developing brain
OT  - Neuroinflammation
OT  - Sevoflurane
EDAT- 2015/08/11 06:00
MHDA- 2015/08/11 06:01
PMCR- 2015/08/01
CRDT- 2015/08/11 06:00
PHST- 2014/05/09 00:00 [received]
PHST- 2014/06/04 00:00 [revised]
PHST- 2014/06/27 00:00 [accepted]
PHST- 2015/08/11 06:00 [entrez]
PHST- 2015/08/11 06:00 [pubmed]
PHST- 2015/08/11 06:01 [medline]
PHST- 2015/08/01 00:00 [pmc-release]
AID - 10.4097/kjae.2015.68.4.397 [doi]
PST - ppublish
SO  - Korean J Anesthesiol. 2015 Aug;68(4):397-401. doi: 10.4097/kjae.2015.68.4.397. 
      Epub 2015 Jul 28.