[The role of activation of nuclear factor-kappa B on the expression of heme oxygenase-1 induced by lipopolysaccharide in rat myocardium].

AIM

The 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.

METHODS

The 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.

CONCLUSION

NF-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.