PMID- 17041734
OWN - NLM
STAT- MEDLINE
DCOM- 20080103
LR  - 20161124
IS  - 0371-0874 (Print)
IS  - 0371-0874 (Linking)
VI  - 58
IP  - 5
DP  - 2006 Oct 25
TI  - Carbon monoxide inhalation protects lung from lipopolysaccharide-induced injury 
      in rat.
PG  - 483-9
AB  - Carbon monoxide (CO), a metabolite of heme catalysis by heme oxygenase (HO), has 
      been proposed to have anti-oxidative, anti-inflammatory and anti-apoptotic 
      functions. Lipopolysaccharide (LPS)-induced lung injury (LI) is characterized by 
      oxidative stress, inflammatory reaction and excessive pulmonary cell apoptosis. 
      So we supposed that CO might have protection against LI. LI in rats was induced 
      by intravenous injection of LPS (5 mg/kg). To observe the effect of CO 
      inhalation, LI rats were exposed to 2.5 x 10(-4) (V/V) CO for 3 h. CO-induced 
      changes of lung oxidative stress parameters, inflammatory cytokines, cell 
      apoptosis, HO-1 expression and histology were examined. Results revealed that 
      expressions of the tumor necrosis factor-alpha (TNF-alpha) and interlukin-6 
      (IL-6), activities of maleic dialdehyde (MDA) and myeloperoxidase (MPO), and cell 
      apoptosis in LPS injection + CO inhalation group were (0.91+/-0.25) pg/mg 
      protein, (0.64+/-0.05) pg/mg protein, (1.02+/-0.23) nmol/mg protein, 
      (7.18+/-1.62) U/mg protein and (1.60+/-0.34)%, respectively, significantly lower 
      than the corresponding values in LI group [(1.48+/-0.23) pg/mg protein, 
      (1.16+/-0.26) pg/mg protein, (1.27+/-0.33) nmol/mg protein, (8.16+/-1.49) U/mg 
      protein and (3.18+/-0.51) %, P<0.05]. Moreover, CO inhalation obviously increased 
      the expressions of HO-1 and interlukin-10 (IL-10) and activity of superoxide 
      dismutase (SOD) [(5.43+/-0.92), (0.26+/-0.07) pg/mg protein and (60.09+/-10.21) 
      U/mg protein in LPS injection + CO inhalation group vs (3.08+/-0.82), 
      (0.15+/-0.03) pg/mg protein and (50.98+/-6.88) U/mg protein in LI group, P<0.05]. 
      LI was attenuated by CO inhalation. Our study demonstrates that inhalation of low 
      concentration of CO protects lung against LPS-induced injury via anti-oxidant, 
      anti-inflammation, anti-apoptosis and up-regulation of HO-1 expression.
FAU - Liu, Shao-Hua
AU  - Liu SH
AD  - Intensive Care Unit, The First Affiliated Hospital of Nanjing Medicial 
      University, Nanjing 210029, China. Liush67@hotmail.com
FAU - Ma, Ke
AU  - Ma K
FAU - Xu, Bing
AU  - Xu B
FAU - Xu, Xin-Rong
AU  - Xu XR
LA  - eng
PT  - Journal Article
PL  - China
TA  - Sheng Li Xue Bao
JT  - Sheng li xue bao : [Acta physiologica Sinica]
JID - 20730130R
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 7U1EE4V452 (Carbon Monoxide)
RN  - 9061-29-4 (Carboxyhemoglobin)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
SB  - IM
MH  - Administration, Inhalation
MH  - Animals
MH  - Apoptosis/drug effects
MH  - Carbon Monoxide/*administration & dosage
MH  - Carboxyhemoglobin/analysis
MH  - Cytokines/biosynthesis
MH  - Heme Oxygenase-1/genetics
MH  - Lipopolysaccharides/*toxicity
MH  - Lung/*drug effects/metabolism/pathology
MH  - Male
MH  - Oxidative Stress/drug effects
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2006/10/17 09:00
MHDA- 2008/01/04 09:00
CRDT- 2006/10/17 09:00
PHST- 2006/10/17 09:00 [pubmed]
PHST- 2008/01/04 09:00 [medline]
PHST- 2006/10/17 09:00 [entrez]
PST - ppublish
SO  - Sheng Li Xue Bao. 2006 Oct 25;58(5):483-9.