Effect of rosuvastatin on expression of angiotensin Ⅱ receptors in rat aortic endothelium after balloon injury

Background It＇s established that Angiotensin Ⅱ and its receptors are involved in intimal hyperplasia after balloon injury and stent restenosis. Recent evidence also suggests that statins have some anti-intimal hyperplasia effects. In this study, the effect of Rosuvastatin on expression of angiotensin Ⅱ receptors in rat aortic endothelium after balloon injury is therefore investigated. Methods All 52 Wistar Kyoto rats were established to aorta injury models by 2F balloon catheter, then were randomly divided into sham operation group, aorta injury group and Rosuvastatin-treatment group. After 14 days, the aortic specimens of the animals were harvested and performed immunohistochemistry and determination of molecular biology. Results The results showed that （i） The 14 days-balloon injury induced obvious intima thickening （P 〈 0.01）, however, the phenomenon was reduced by 14 daystreatment with Rosuvastatin （P 〈 0.01）. （ii） The expressions of angiotention Ⅱ type Ⅰ （AT1） and type Ⅱ （AT2） receptor mRNA and protein were markedly up-regulated by the balloon injury （P 〈 0.01）, after 14 days-treatment with Rosuvastatin, the expression of AT1 receptor mRNA and its protein was decreased （P 〈 0.01）, but the expression of AT2 receptor mRNA and its protein was further increased （P 〈 0.05）. Conclusion In this study, we observed that the balloon injury induced-intima thickening was reduced by Rosuvastatin in rats, which might be linked with the regulation of expression of angiotensin Ⅱ receptors.

Heparin-derived oligosaccharide inhibits vascular intimal hyperplasia in balloon-injured carotid artery

The aims of the present study were to determine the effects of heparin-derived oligosaccharides(HDOs) on vascular intimal hyperplasia(IH) in balloon-injured carotid artery and to elucidate the underlying mechanisms of action. An animal model was established by rubbing the endothelia within the common carotid artery(CCA) in male rabbits. The rabbits were fed a high-cholesterol diet. Arterial IH was determined by histopathological changes to the CCA. Serum lipids were detected using an automated biochemical analysis. Expressions of mR NAs for vascular endothelial growth factor(VEGF), basic fibroblast growth factor(bF GF), vascular cell adhesion molecule-1(VCAM-1), monocyte chemoattractant protein-1(MCP-1), scavenger receptor class B type I(SR-BI), and ATP-binding cassette transporter A1(ABCA-1) were analyzed using reverse transcription polymerase chain reaction assays. Expressions of VEGF, VCAM-1, MCP-1, SR-BI and ABCA-1 proteins were analyzed by Western blotting. Enzyme-linked immunosorbent assays were used to quantify expression levels of VEGF and b FGF. Our results showed that administration of HDO significantly inhibited CCA histopathology and restenosis induced by balloon injury. The treatment with HDOs significantly decreased the m RNA and protein expression levels of VEGF, b FGF, VCAM-1, MCP-1, and SR-BI in the arterial wall; however, ABCA-1 expression level was elevated. HDO treatment led to a reduction in serum lipids(total cholesterol, triglycerides, high-density and low-density lipoproteins). Our results from the rabbit model indicated that HDOs could ameliorate IH and underlying mechanism might involve VEGF, b FGF, VCAM-1, MCP-1, SR-BI, and ABCA-1.