期刊文献+

血管紧张素-Ⅱ对血管内皮细胞内皮素-1 mRNA表达水平的影响及阿托伐他汀的保护作用 被引量:2

Effects of Ang-Ⅱ on the Expression of Endothelin-1 mRNA and the protection of Atorvastatin in vascular endothelial cell
暂未订购
导出
摘要 目的观察血管紧张素(Ang)-Ⅱ对血管内皮细胞内皮素(ET)-1 mRNA表达水平的影响及阿托伐他汀的保护作用。方法将培养的血管内皮细胞随机分为4组:空白对照组(仅给予细胞培养液)、单纯Ang-Ⅱ组(细胞培养液中加入Ang-Ⅱ,使其终浓度为10-7mol/L)、Ang-Ⅱ+小剂量阿托伐他汀组(在单纯Ang-Ⅱ组的基础上加入阿托伐他汀,使阿托伐他汀的终浓度为0.1μmol/L)、Ang-Ⅱ+大剂量阿托伐他汀组(在单纯Ang-Ⅱ组的基础上加入阿托伐他汀,使阿托伐他汀的终浓度为1μmol/L)。以反转录-聚合酶链反应(RT-PCR)方法检测血管内皮细胞的ET-1mRNA表达水平。结果①与空白对照组相比,单纯Ang-Ⅱ组血管内皮细胞的ET-1 mRNA表达水平显著增高(P<0.01);②与单纯Ang-Ⅱ组相比,两个Ang-Ⅱ+阿托伐他汀组大鼠的心肌ET-1 mRNA表达水平显著降低(P<0.01);③Ang-Ⅱ+高浓度阿托伐他汀组的ET-1 mRNA表达水平显著低于Ang-Ⅱ+低浓度阿托伐他汀组(P<0.05)。结论Ang-Ⅱ可使血管内皮细胞ET-1 mRNA表达水平显著增高,阿托伐他汀可逆转这一作用,且其作用呈剂量依赖性。 Objective To investigate the effects of Ang-Ⅱ on the expression of endothelin (ET)-1 mRNA and the protection effect of Atorvastatin in Vascular Endothelial Cell (VEC). Methods Cultured VEC were divided into 4 groups: control group (only given cell culture medium) ; Ang-Ⅱ group (given Ang-Ⅱ with the final concentration be 10^- 7 mol/L) ; Ang-Ⅱ + low de, sage atorvastatin group (atorvastatin were given with the final concentration be 0.1 μmol/L at the base of Ang-Ⅱ group; Ang-Ⅱ + high dosage atorvastatin group (atorva.statin were given with the final concentration be 1 μmol/L at the base of Ang-Ⅱ group). The expression of ET-1 mRNA was evaluated by RT-PCR. Results ①The expression level of ET-1 mRNA in Ang-Ⅱ group is significantly higher than that of control group (P 〈 0.01 ) ; ②The expression level of ET-1 mRNA in Ang-Ⅱ + atorvastatin group is significantly lower than that orang- Ⅱ group ( P〈0.01 ) ; ③The exprexsion level of ET-1 mRNA in Ang-Ⅱ + high dosage atorvastatin group is significantly lower than that of Ang- Ⅱ + low dosage atorvastatin group ( P 〈 0.05). Conclusion Ang-Ⅱ increases the expression of ET-1 mRNA in VEC, Atorvastatin inhibits the expression of ET-1 mRNA in a dose-dependent manner.
出处 《山西医药杂志(上半月)》 CAS 2008年第9期771-773,共3页 Shanxi Medical Journal
基金 海军后勤科研基金资助项目(00-3321)
关键词 血管紧张素 阿托伐他汀 内皮素-1 Angiotensin- Ⅱ Atorvastatin Endothelin-1
  • 相关文献

参考文献9

二级参考文献46

  • 1张铖,叶平,陈国林.吡格列酮对压力负荷引起大鼠心肌肥厚的抑制作用[J].中国动脉硬化杂志,2004,12(3):313-316. 被引量:10
  • 2Nishikawa H,Miura S,Zhang B,et al.Statins induce the regression of left ventricular mass in patients with angina.Circ J,2004,68:121-125.
  • 3Landrier JF,Thomas C,Grober J,et al.Statin induction of liver fatty acid-binding protein (L-FABP) gene expression is peroxisome proliferator-activated receptor-alpha-dependent.J Biol Chem,2004,279:45512-45518.
  • 4Simpson P,McGratha A,Savion S.Myocyte hypertrophy in neonatal rat heart cultures and its regulation by serum and by cate2 cholamines.Circ Res,1982,51:787-801.
  • 5Shioi T,Matsumori A,Kihara Y,et al.Increased expression of interleukin-1 beta and monocyte chemotactic and activating factor/monocyte chemoattractant protein-1 in the hypertrophied and failing heart with pressure overload.Circ Res,1997,81:664-671.
  • 6Sakata Y,Yamamoto K,Mano T,et al.Activation of matrix metalloproteinases precedes left ventricular remodeling in hypertensive heart failure rats:its inhibition as a primary effect of Angiotesin-converting enzyme inhibitor.Circulation,2004,109:2143-2149.
  • 7Coker ML,Doscher MA,Thomas CV,et al.Matrix metalloproteinase synthesis and expression in isolated LV myocyte preparations.Am J Physiol,1999,277(2 Pt 2):H777-H787.
  • 8Hasegawa H,Yamamoto R,Takano H,et al.3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors prevent the development of cardiac hypertrophy and heart failure in rats.J Mol Cell Cardiol,2003,35:953-960.
  • 9Patel R,Nagueh SF,Tsybouleva N,et al.Simvastatin induces regression of cardiac hypertrophy and fibrosis and improves cardiac function in a transgenic rabbit model of human hypertrophic cardiomyopathy.Circulation,2001,104:317-324.
  • 10Zhao SP,Zhang DQ.Atorvastatin reduces interleukin-6 plasma concentration and adipocyte secretion of hypercholesterolemic rabbits.Clin Chim Acta,2003,336:103-108.

共引文献63

同被引文献11

引证文献2

二级引证文献5

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