Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-1-9
pubmed:abstractText
To study the production NO by macrophages (M phi) after burn injury and the possible mechanism, we determined the NO production and the iNOS (inducible NO synthase) activity of peritoneal M phi (PM phi) in scald mouse, and the effect of iNOS specific blocker NMMA. Actinomycin D (AD) and protein tyrosine kinase (PTK), special inhibitor Genisteinon them in vitro. It was found that PM phi produced excessive NO in the early postburn phase and the iNOS activity was increased significantly, and there was a positive correlation between them. NMMA, AD as well as Genistein could inhibit the NO production, the activity of iNOS was decreased by both AD and Genistein. The results suggested that M phi was activated after thermal injury and it could produce NO excessively through initiating iNOS synthesis. PTK signal system was involved in the NO production by M phi via affecting the iNOS synthesis after burn injury.
pubmed:language
chi
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1000-7806
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
268-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
[The role of thermal injury on nitric oxide (NO) production by mouse macrophages and its possible mechanism].
pubmed:affiliation
Burn Research Institute, Southwestern Hospital, Third Military Medical College, Chongqing.
pubmed:publicationType
Journal Article, English Abstract, Research Support, Non-U.S. Gov't