The aim of this paper was to study the curative effect of Huotan Jiedu
Tongluo (HTJDTL) decoction on a rabbit model with early
atherosclerosis (AS),and furtherly to explore whether it could inhibit the BH4/eNOS uncoupling ROS or not. Twenty-four Japanese white rabbits were randomly divided into
sham operation group, model group, HTJDTL decoction group and
atorvastatin group. Rabbit models with early
atherosclerosis were established by high fat diet,
nitrogen drying and carotid artery balloon injury. The rabbits were sacrificed at 7th days after balloon injury and several parameters were measured. The pathological morphology of the common carotid artery was observed by HE staining. The blood
lipids were detected by
peroxidase method. The ratio of vascular eNOS dimer and monomer was measured by Western blot. The ELISA and biochemical technology were respectively used for testing BH4 and ROS levels in serum. The results showed that compared with the
sham operation group, the model group had mild
stenosis of the common carotid artery lumen, uneven intimal
hyperplasia,
lipid deposition in the intima and media, and obvious
hyperplasia of the adventitia with inflammatory cell infiltration. The HTJDTL decoction could significantly inhibit the intimal
hyperplasia compared with the model group, meanwhile, reduce the
lipid deposition of the media and the infiltration of the adventitial cells. Compared with the
sham operation group, the blood
lipids and ROS of the model animals significantly increased, but BH4 and the ratio of eNOS dimer/monomer decreased. Compared with the model group, HTJDTL decoction significantly reduced the TC,
ox-LDL and ROS levels, and also up-regulated eNOS dimer/monomer ratio, but it increased BH4 trend without statistical difference. According to the results, it was found that HTJDTL decoction couldsignificantly prevent and improve the
vascular remodeling of rabbits model with early
atherosclerosis. The mechanism of decoction may largely be related to the inhibition of BH4/eNOS uncoupling and the reduction of oxidative stress.