PMID- 22791148
OWN - NLM
STAT- MEDLINE
DCOM- 20121218
LR  - 20220310
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 35
IP  - 7
DP  - 2012
TI  - An exogenous hydrogen sulphide donor, NaHS, inhibits the nuclear factor kappaB 
      inhibitor kinase/nuclear factor kappab inhibitor/nuclear factor-kappaB signaling pathway 
      and exerts cardioprotective effects in a rat hemorrhagic shock model.
PG  - 1029-34
AB  - Hemorrhagic shock (HS) is a common condition and leading cause of death in trauma 
      patients universally. Severe inflammatory responses during HS finally lead to 
      multiple-organ failure. Hydrogen sulphide (H(2)S) is increasingly recognized as an 
      important signaling molecule with various protective effects. In the present 
      study, we investigated the antiinflammatory and cardioprotective effects of an 
      exogenous H(2)S donor, sodium hydrosulfide (NaHS), in an HS rat model. Male 
      Sprague-Dawley rats were randomly divided into the sham-operated, sham-operated 
      treated with NaHS (28 micromol/kg, intraperitoneally (i.p.)), HS, and HS treated with 
      NaHS (28 micromol/kg, i.p.) groups. The HS groups were subjected to mimicked HS for 
      1 h and then treated with NaHS or left untreated. The rats were then resuscitated 
      with Ringer lactate solution for 1 h. Myocardial enzymes and inflammatory 
      cytokines were evaluated. Morphologic changes in cardiac tissue and 
      ultrastructural injury were also analyzed. HS resulted in significant hemodynamic 
      deterioration and increased myocardial enzyme and inflammatory cytokine levels. 
      Intraperitoneal administration of NaHS significantly prevented hemodynamic 
      deterioration and decreased the elevation of myocardial enzymes. NaHS also 
      inhibited the nuclear factor kappaB inhibitor kinase (IKK)/nuclear factor kappaB 
      inhibitor (IkappaB)/nuclear factor kappaB (NF-kappaB) signaling pathway. The results suggest 
      that NaHS exerts cardioprotective effects against HS. The protective effects of 
      NaHS may occur via down-regulation of the IKK/IkappaB/NF-kappaB signaling pathway.
FAU - Gao, Cao
AU  - Gao C
AD  - Department of Anesthesiology, Tangdu Hospital, Fourth Military Medical 
      University, Xi'an 710032, P. R. China.
FAU - Xu, Dun-Quan
AU  - Xu DQ
FAU - Gao, Chang-Jun
AU  - Gao CJ
FAU - Ding, Qian
AU  - Ding Q
FAU - Yao, Li-Nong
AU  - Yao LN
FAU - Li, Zhi-Chao
AU  - Li ZC
FAU - Chai, Wei
AU  - Chai W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Cardiotonic Agents)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Sulfides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.1.1.27 (L-Lactate Dehydrogenase)
RN  - EC 2.7.11.10 (I-kappa B Kinase)
RN  - EC 2.7.3.2 (Creatine Kinase)
RN  - FWU2KQ177W (sodium bisulfide)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
MH  - Animals
MH  - Cardiotonic Agents/*pharmacology
MH  - Creatine Kinase/blood
MH  - Disease Models, Animal
MH  - Hydrogen Sulfide/metabolism
MH  - I-kappa B Kinase/*antagonists & inhibitors/metabolism
MH  - I-kappa B Proteins/*antagonists & inhibitors/metabolism
MH  - Interleukin-6/blood
MH  - L-Lactate Dehydrogenase/blood
MH  - Male
MH  - NF-kappa B/*antagonists & inhibitors/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Shock, Hemorrhagic/*metabolism
MH  - Signal Transduction/drug effects
MH  - Sulfides/*pharmacology
MH  - Tumor Necrosis Factor-alpha/blood
EDAT- 2012/07/14 06:00
MHDA- 2012/12/19 06:00
CRDT- 2012/07/14 06:00
PHST- 2012/07/14 06:00 [entrez]
PHST- 2012/07/14 06:00 [pubmed]
PHST- 2012/12/19 06:00 [medline]
AID - DN/JST.JSTAGE/bpb/b110679 [pii]
AID - 10.1248/bpb.b110679 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2012;35(7):1029-34. doi: 10.1248/bpb.b110679.