The role of activation of nuclear factor-kappa B on the expression of heme oxygenase-1 induced by lipopolysaccharide in rat myocardium.
- Author:
Xiao-Yun ZHAO
1
;
Yu-Guang LI
;
Qing WANG
;
Xue GUO
;
Dong-Hui ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Heme Oxygenase-1; genetics; metabolism; Lipopolysaccharides; adverse effects; Male; Myocardium; metabolism; NF-kappa B; metabolism; Rats; Rats, Sprague-Dawley; Shock, Septic; metabolism
- From: Chinese Journal of Applied Physiology 2006;22(1):54-57
- CountryChina
- Language:Chinese
-
Abstract:
AIMThe role of activated nuclear factor-kappa B(NF-kappaB) on the expression of heme oxygenase-1 induced by lipopolysaccharide (LPS) in rats' myocardium was obversed, and the effect exerted in endotoxic shock was explored.
METHODSThe changes in mean arterial pressure within 12 hours were recorded on a polygraph. The protein expression of NF-kappaB p65 in rats'myocardium, which were induced by lipopolysaccharide were measured with immunochemistry. The changes both of protein and gene expression of heme oxygenase-1 in rats' myocardium, which were induced by injection of LPS or preadministration of the specific inhibitor of NF-kappaB, pyrrolidine dithiocarbamate(PDTC), were examined by immunochemistry of reverse transcripted polymerase chain reaction.
RESULTS(1) LPS caused a rapid decrease of MAP within 12 h( P < 0.01). (2) After LPS was administration, the protein expression of NF-kappaB p65 in both of micrangium endothelium within myocardium markedly increased at 0.5 h and 2 h, while decreased gradually at 6 h and 12 h. (3) ES group expressed as migration of acute inflammatory cells and dilation and stagnation in blood capillary, while the increase of HO-1 mRNA induced by LPS didn't change at the first 0.5 h, began at 2 h, peaked at 6 h, and declined at 12 h, respectively. The protein expression of HO-1 in micrangium endothelium within myocardium markedly increased and emerged in myocardium, and kept a high level at 6 h and 12 h. (4) When a specific inhibitor of NF-kappaB, PDTC, was applied to inhibit the level of NF-kappaB, we found that the pathomorphological changes of myocardium in ES rats were improved and both HO-1 mRNA and protein expression in myocardium markedly failed at 6 h.
CONCLUSIONNF-kappaB was activated on the stimulation of LPS, which brought about its translocation to the nucleus to act on transcription activity of HO-1 gene. NF-kappaB might be involved in its signal transductive mechanisms, which might be one of the important mechanism of LPS inducing the refractory low arterial pressure in ES rats.