[The role of thermal injury on nitric oxide (NO) production by mouse macrophages and its possible mechanism].
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.
Luo
G
G
Burn Research Institute, Southwestern Hospital, Third Military Medical College, Chongqing.
Peng
D
D
Huang
W
W
D000818:Animals; D002056:Burns / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D017737:Macrophages, Peritoneal / Q000378:metabolism*; D051379:Mice; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D019323:omega-N-Methylarginine / Q000494:pharmacology
D004791:Enzyme Inhibitors; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase