期刊文献+

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

Effect of rosuvastatin on expression of angiotensin Ⅱ receptors in rat aortic endothelium after balloon injury
原文传递
导出
摘要 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. 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.
出处 《South China Journal of Cardiology》 CAS 2011年第1期49-55,共7页 岭南心血管病杂志(英文版)
基金 supported by Science and Technology Bureau of Qingdao City (Grant No. 02-2-kj-yn-25)
关键词 ROSUVASTATIN balloon injury angiotention receptor rosuvastatin balloon injury angiotention Ⅱ receptor
  • 相关文献

参考文献9

  • 1唐兵,何国祥,李德,刘建平,景涛.AT2R基因在体转染抑制大鼠颈动脉新生内膜增生[J].中国病理生理杂志,2007,23(2):297-302. 被引量:3
  • 2王安才,成蓓,谢晓竟,徐浩.阿托伐他汀对自发性高血压大鼠心室重构的影响[J].中国临床药理学与治疗学,2004,9(8):880-884. 被引量:32
  • 3Yong Meng,,Fang Li, et al.The study progress of An-giotensin Ⅱ receptor in the heart protection. Advances InCardiovascular Diseases . 2007
  • 4Seljeflot I,Tonstad S,Hjermann I,et al.Reduced expression of endothelial cell markers after 1 year treatment with simvastatin and atorvastatin in patients with coronary heart disease. Atherosclerosis . 2002
  • 5Ichiki T,Takeda K,Tokunou T,et al.Downregulation of angiotensin II type 1 receptor by hydrophobic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors in vascular smooth muscle cells. Arteriosclerosis . 2001
  • 6Nakata S,Tsutsui M,Shimokawa H,et al.Statin treat-ment upregulates vascular neuronal nitric oxide synthase through Akt/NF-kappa B pathway. Arteriosclerosis and Thrombosis . 2007
  • 7Libby P,Aikawa M.Mechanisms of plaque stabilization with statins. The American Journal of Cardiology . 2003
  • 8Rudijanto A.The role of vascular smooth muscle cells on the patho-genesis of atherosclerosis. Acta Med Indones . 2007
  • 9Iwai M,Chen R,Li Zet al.Deletion of angiotensinⅡtype2receptor exaggerated atherosclerosis in apolipoprotein E-null mice. Circulation . 2005

二级参考文献18

  • 1[1]O'Driscoll G, Green D, Taylor RR. Simvastatin, an HMG-coenzyme A reductase inhibitor, improves endothelial function within 1 months[J]. Circulation, 1997;95(5):1126-31
  • 2[2]Osamah H, Mira R, Sorina S, Shlomo K, Michael A. Reduced platelet aggregation after fluvastatin therapy is associated with altered platelet lipid composition and drug binding to the platelets [J]. Br J Clin Pharmacol, 1997;44(1):77- 83
  • 3[3]Ridker PM, Rifai N, Marc A, Pfeffer MA, Sacks F, Braunwald E. Long-term effects of pravastatin on plasma concentration of C-reactive protein. The cholesterol and recurrent events (CARE) investigators[ J]. Circulation, 1999; 100(3): 230 - 5
  • 4[4]Guijarro C, Blanco-Colio LM, Ortego M, Alonso C, Ortiz A,Plaza JJ, et al. 3-hydroxy-3-methylglutaryl coenzyme A reductase and isoprenylation inhibitors induce apoptosis of vascular smooth muscle cells in culture[J]. Circ Res, 1998;83(5) :490- 500
  • 5[5]Wassmann S, Laufs U, Baumer AT, Muller K, Ahlbory K,Linz W, et al. HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species[J]. Hypertension,2001 ;37(6): 1450 - 7
  • 6[6]Wong B, Lumma WC, Smith AM, Sisko JT, Wright SD, Cai TQ. Statins suppress THP-1 cell migration and secretion of matrix metalloproteinase 9 by inhibiting geranylgeranyllation 3 [J].J Leukoc Biol, 2001 ;69(6) :959 - 62
  • 7[7]Su SF, Hsiao CL, Chu CW, Lee BC, Lee TM. Effects of pravastatin on left ventricular mass in patients with hyperlipidemia and essential hypertension [ J ]. Am J Cardiol, 2000; 86(5):514-8
  • 8[8]Patel R, Nagueh SF, Tsybouleva N, Abdellatif M, Lutucuta S,Kopelen HA, et al. Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopthy [J]. Circulation, 2001; 104(3) :317 - 24
  • 9[10]Sadoshima JI, Izumo S. Molecular characterization of angiotensin Ⅱ -induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts[J]. Circ Res, 1993;73(3):413 - 23
  • 10[11]Sadoshima J, Xu Y, Slayter HS, Izumo S. Autocrine release of angiotensin Ⅱ mediates stretch-induced hypertrophy of cardiac myocytes in vitro[J]. Cell, 1993;75(5) :977 - 84

共引文献32

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部