Abstract: NFκB is a transcription factor regulating many
function of the vessel wall. In the normal condition , NFκB is
revealed diffuse cytoplasmic expressionsuggesting that the system is
inactive. The presence of activation NFκB provide a potential
pathway for the rapid transcriptional of a variety of genes encoding
cytokines, growth factors, adhesion molecules and procoagulatory
factors. It is likely to play an important role in chronic inflamatory
disease involved atherosclerosis. There are many stimuli with the
potential to active NFκB, including hyperlipidemia. We used 24 mice
which was divided in 6 groups. The HFD given by et libitum
procedure during 2, 4, and 6 months. The parameters in this study
were the amount of NFKB activation ,H2O2 as ROS and VCAM-1 as
a product of NFKB activation. H2O2 colorimetryc assay performed
directly using Anti Rat H2O2 ELISA Kit. The NFKB and VCAM-1
detection obtained from aorta mice, measured by ELISA kit and
imunohistochemistry. There was a significant difference activation of
H2O2, NFKB and VCAM-1 level at induce HFD after 2, 4 and 6
months. It suggest that HFD induce ROS formation and increase the
activation of NFKB as one of atherosclerosis marker that caused by
hyperlipidemia as classical atheroschlerosis risk factor.