Key result
Salusin-α gene overexpression reduces vascular intimal thickness and improves lipid profiles in atherosclerotic rabbits.
Why the study?
Inhibiting vascular endothelial foam formation is a clinical focus, but the effects of salusin-α gene overexpression on vascular intimal hyperplasia in atherosclerosis are not fully understood.
Does salusin-α gene overexpression inhibit vascular intimal hyperplasia in an atherosclerotic rabbit model?
Does salusin-α gene overexpression inhibit vascular intimal hyperplasia in an atherosclerotic rabbit model?
p-value: p=< 0.05
Overexpression of the salusin-α gene inhibits vascular intimal hyperplasia and improves lipid profiles in an atherosclerotic rabbit model, suggesting a potential mechanism for preventing vascular intimal cell foaming.
Hypothesis-generating for salusin-α in atherosclerosis; leaves open translation to human therapy.
Inhibiting vascular endothelial foam is the focus of clinical attention. Using SonoVue (an ultrasound contrast agent), the salusin-α 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-α gene overexpression (P) group were higher than those in the salusin-α gene interference (RP) group (P < 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 (P < 0.05). The expression of positive regulators of atherosclerosis (ABCA1, ABCG1) was higher in the P group than that in the RP group (P < 0.05), and the opposite effect was observed for negative regulators (ACAT1, CD36). Thus, our results showed that the overexpression of salusin-α gene inhibited the proliferation of the vascular intima, thereby throwing some light on understanding the mechanism how salusin-α gene expression interfered with the foaming of vascular intimal cells.
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Qian et al. (2018) studied Atherosclerosis. Salusin-α gene overexpression vs. Salusin-α gene interference was evaluated on Vascular intimal thickness (p=< 0.05). Overexpression of the salusin-α gene significantly reduced vascular intimal thickness and improved lipid profiles compared to gene interference in an atherosclerotic rabbit model (P < 0.05).
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