PMID- 19557603
OWN - NLM
STAT- MEDLINE
DCOM- 20090811
LR  - 20090626
IS  - 0955-3002 (Print)
IS  - 0955-3002 (Linking)
VI  - 85
IP  - 7
DP  - 2009 Jul
TI  - Static magnetic field attenuates mortality rate of mice by increasing the 
      production of IL-1 receptor antagonist.
PG  - 633-40
LID - 10.1080/09553000902993908 [doi]
AB  - PURPOSES: Disseminated intravascular coagulation (DIC) is a complex systemic 
      thrombohemorrhagic disorder involving intravascular coagulation and hemorrhage. 
      The aim of this study is to test whether static magnetic field (SMF) is effective 
      in attenuating lipopolysaccharide (LPS)-induced DIC. MATERIALS AND METHODS: In 
      vivo experiments were performed in this study using male BALB/cByJ mice. An 
      intraperitoneal injection of 50 mg/kg LPS was shown to lead to approximately 50% 
      mortality and this dose was used in subsequent experiments. To test the effects 
      of SMF on the survival rate of LPS-induced animals, the mice were exposed to 
      0.25-T SMF for 2 h before LPS injection. In addition, the effect of a 2-h SMF 
      treatment on the production of anti-inflammatory cytokines was evaluated. 
      RESULTS: In the first set of experiments, we found that the survival rate was 
      higher in the SMF-exposed group than in the sham-exposed group. The circulating 
      platelet (PLT) counts in the SMF-exposed mice were significantly higher than in 
      the unexposed animals. However, no significant changes in inflammatory cytokine, 
      including tumour necrosis factor-alpha (TNF-alpha), interleukin-1alpha 
      (IL-1alpha), interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1), in 
      plasma were found after SMF treatment. The results from the second experiment 
      showed that the plasma levels of interleukin-1 receptor antagonist (IL-1ra) were 
      higher in the SMF-exposed group than in the sham group. CONCLUSIONS: Exposure to 
      an SMF increases the plasma levels of IL-1ra. This effect may inhibit the 
      reduction in PLT in plasma, resulting in prevention in LPS induced DIC.
FAU - Lin, Shu-Li
AU  - Lin SL
AD  - Dental Department, Cathay General Hospital, Taipei, Taiwan.
FAU - Chang, Wei-Jen
AU  - Chang WJ
FAU - Lin, Yung-Sheng
AU  - Lin YS
FAU - Ou, Keng-Liang
AU  - Ou KL
FAU - Lin, Che-Tong
AU  - Lin CT
FAU - Lin, Chih-Ping
AU  - Lin CP
FAU - Huang, Haw-Ming
AU  - Huang HM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Int J Radiat Biol
JT  - International journal of radiation biology
JID - 8809243
RN  - 0 (Interleukin 1 Receptor Antagonist Protein)
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Animals
MH  - Disseminated Intravascular Coagulation/*mortality
MH  - Interleukin 1 Receptor Antagonist Protein/*biosynthesis
MH  - Lipopolysaccharides/toxicity
MH  - *Magnetics
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Platelet Count
EDAT- 2009/06/27 09:00
MHDA- 2009/08/12 09:00
CRDT- 2009/06/27 09:00
PHST- 2009/06/27 09:00 [entrez]
PHST- 2009/06/27 09:00 [pubmed]
PHST- 2009/08/12 09:00 [medline]
AID - 912685984 [pii]
AID - 10.1080/09553000902993908 [doi]
PST - ppublish
SO  - Int J Radiat Biol. 2009 Jul;85(7):633-40. doi: 10.1080/09553000902993908.