Overexpression of Salusin- Inhibits Vascular Intimal Hyperplasia in an Atherosclerotic Rabbit Model.

Inhibiting vascular endothelial foam is the focus of clinical attention. Using SonoVue (an ultrasound contrast agent), the salusin- gene was transfected into the arterial intima of an atherosclerotic rabbit model induced by a high-fat diet in this study. Subsequently the model of blood lipid indexes, the pathological structure of the intima, and changes in molecules regulating atherosclerosis were investigated. The high-density lipoprotein C and apolipoprotein A values in the salusin- gene overexpression (P) group were higher than those in the salusin- gene interference (RP) group ( < 0.05), whereas the total cholesterol, low-density lipoprotein C, and apolipoprotein B values were reversed. Rabbits in the P group showed significantly thinner vascular intimal thickness than that of other experimental groups ( < 0.05). The expression of positive regulators of atherosclerosis (, ) was higher in the P group than that in the RP group ( < 0.05), and the opposite effect was observed for negative regulators (, ). Thus, our results showed that the overexpression of salusin- gene inhibited the proliferation of the vascular intima, thereby throwing some light on understanding the mechanism how salusin- gene expression interfered with the foaming of vascular intimal cells.