我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

辛伐他汀对动脉粥样硬化斑块中MMPs 及TIMPs 表达的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2003年第6期
页码:
513-515
栏目:
实验研究
出版日期:
2003-11-01

文章信息/Info

Title:
The effect of Simvastatin on matrix metalloproteinases and its tissue inhibitors expression in atherosclerotic plaques in rabbits
作者:
张斌; 韦方; 耿庆山; 靳立军; 冯建章; 余细勇
广东省心血管病研究所心内科, 广东 广州 510100
Author(s):
ZHANG Bin;  WEI Fang;  GENG Qing-shan;  JIN Li-jun;  FENG Jian-zhang;  YU Xi-yong
Department of Cardiology, Guangdong Provincial Cardiovascular Institute, Guangzhou, Guangdong 510100, China
关键词:
辛伐他汀; 金属蛋白酶; 金属蛋白酶组织抑制因子
Keywords:
Simvastatin;  matrix metalloproteinases;  tissue inhibitors of metalloproteinases
分类号:
R541.4,Q75　
DOI:
-
文献标识码:
A
摘要:
目的:观察辛伐他汀对动脉粥样硬化斑块中基质金属蛋白酶(MMPs)及其组织抑制因子(TIMPs)表达的影响。方法:新西兰大白兔48只随机分为试药组和对照组, 用PTCA球囊导管拉伤腹主动脉, 高脂饮食喂养4周后,试药组(24 只)给予辛伐他汀5 mg·kg- 1·d- 1, 对照组(24只)以淀粉为对照; 每组按实验终点(给药后2、4 和8周) 随机分为3 个亚组, 继续高脂饮食喂养至实验结束。动物高脂喂养前、每周和处死前取静脉血2 ml检测血脂变化, 取拉伤段动脉用于总RNA提取和组织病理检测。结果: 高脂饮食喂养1周后, 2组动物血脂水平在正常的5～10倍, 组间无显著差异(P>0.05); 用药后2周, 试药组血脂明显低于对照组; 用药后4周, 试药组血管组织MMP1, 2 低于对照组, TIMP1/MMP1明显大于对照组(P<0.05, P<0.01), TIMPs 表达两组无显著差异(P>0.05)。结论: 辛伐他汀通过选择性地改变局部MMPs 和TIMPs表达,减少基质分解破坏, 增加局部斑块的稳定性。
Abstract:
AIM: To investigate the effects of Simvastatin on matrix metalloproteinases (MMPs) and its tissue inhibitors of metalloproteinases (TIMPs) expression in atherosclerotic plaques in rabbits. METHODS: 48 New Zealand white rabbits were randomly divided into 2 groups: the experimental group (I) and the control group (?). Abdominal aortas of all the rabbits were injured by PTCA balloon catheter. Then hypercholesterol diet was given. Rabbits in group I were fed on Simvastat in 5 mg/kg per day and placebo was given in group ? since the fifth week. Each group was divided into 3 subgroups according to the sacrifice time (2, 4 and 8 weeks after the administration of Simvastatin). Blood samples and arterials were harvested for further analyses. RE2SULTS: Blood lipids were increased to 5～10 folds after one week’s hypercholesterol diet and maintained at this high level. At the end of 2 weeks, the levels of blood lipids in group I decreased significantly, the expression of MMP1, 2 in group I was lower and the values of TIMP1/MMP1 were higher than those of the control group (P<0.05 or 0.01) 4 weeks after the administration of Simvastatin. CONCLUSION: Simvastatin could increases the stability of atherosclerotic plaque and by specifically changing the local expression of MMPs and the ratio of TIMP/MMP decrease.

参考文献/References

[1] Gruppo Italiano per lo Studio della Sop ravvivenza nell’ Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarctiion [J] . Lancet, 1986, 1:397-401.

[2] Chester MR, Chen L, Kaski JC. Angiographic evidence for frequent " silent" plaque disruption in patients with stable angina(abstract) [J] . J Am Coll Cardiol, 1995, Special Issue:428A.

[3] The LIPID Study Group. design features and baseline characteristics of the LIPID (Long-Term Intervention with Pravastatin in Ischemic D isease) study: a randomized trial in patients with previous acute myocardial infarction and/or unstable angina pectoris [J] . Am J Cardiol, 1995, 76:474-479.

[4] Kipshidze N, Sahota H, Komorowski R, et al. Photo remodeling of arterial wall reduces restenosis after balloon angioplasty in an atherosclerotic rabbit model [J] . J Am Coll Cardiol, 1998, 31:1152-57.

[5] 柳英侠, 毕延发, 张淑芹, 等. 定位性动脉粥样硬化狭窄模型的复制 [J] . 哈尔滨医科大学学报, 1997, 31:161-162.

[6] Ara T, Kusafuka T, Lnoue M, et al. Determination of imbalance between MMP-2 and TIMP-2 in human neuroblastoma by reverse- transcription polymerase chain reaction and its correlation with tumor progression [J] . J Pediatric Surg, 2000, 35:432-437.

[7] Takeba Y, Suzuki N, Taaeno M, et al. Modulation of synovial cell function by somatostatin in patients with rheumatoid arthritis [J] . Arthritis Rheum, 1997, 40:2128-2138.

[8] Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4s) [J] . Lancet, 1994, 344:1383-1389.

[9] Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels [J] . N Engl J Med, 1996, 335:1001-1009.

[10] Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group [see comments] [J] . N Engl J Med , 1995, 333:1301-1307.

[11] Zorina SG. Increased expression of matrix metalloproteinase and matrix degrading activity in vulnerable regions of human atherosclerotic plaques [J] . Clin Invest, 1994, 94:2493-2503.

[12] Soren DP, Erik MP, Steffen R, et al. Coronary artery disease: Plaque vulnerability, disruption, and thrombosis. In: Fuster V. The vulnerable atherosclerotic Plaque [M] . New York: Futura, 1999. 1-23.

备注/Memo

备注/Memo:
收稿日期：2003-03-03.
更新日期/Last Update: 2003-11-01