Introduction
Coronary heart disease (CHD) is a dynamic process in which there are
interactions between endothelial dysfunction, oxidative stress, and
inflammatory responses. The aim of the present study was to investigate the
function and mechanism of HSCARG in the treatment of CHD.
Methods
Male apolipoprotein E/low-density lipoprotein receptor-deficient mice were
given a high-fat diet with 21% fat and 0.15% cholesterol for the in vivo
model. Human umbilical vein endothelial cells were incubated with
angiotensin II for the in vitro model. HSCARG expression was inhibited in
patients or mice with CHD.
Results
HSCARG reduced oxidative stress in mice with CHD. HSCARG also reduced
reactive oxygen species (ROS)-oxidative stress in the in vitro model. HSCARG
induced p47phox expression in the in vitro model by NF-κB activity.
The regulation of nuclear factor kappa B (NF-κB) activity or p47phox
expression participates in the effects of HSCARG in CHD.
Conclusion
Altogether, our data indicate that HSCARG reduced ROS-oxidative stress in in
vivo and in vitro models of CHD via p47phox by NF-κB activity and may
be a clinical target for CHD.
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