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|

诱导型环氧合酶高表达增加兔主动脉粥样硬化斑块易损性

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2011年第6期
页码:
715-718
栏目:
基础研究
出版日期:
2011-12-25

文章信息/Info

Title:
Overexpression of COX-2 enhances rabbit atherosclerotic plaque vulnerability
作者:
李 岚1; 樊 民2; 倪灿荣3; 梁 春2; 任雨笙2; 吴宗贵2
1.解放军第411医院内四科，上海 200081；2.第二军医大学长征医院心内科， 上海 200003；3.第二军医大学长海医院病理科,上海 200433
Author(s):
LI Lan1;  FAN Min2;  NI Can-rong3;  LIANG Chun2;  REN Yu-sheng2;  WU Zong-gui2
1.Fourth Medical Department, PLA 411 Hospital, Shanghai 200081, China; 2.Department of Cardiovasology, Changzheng Hospital, 3.Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai 200003, China
关键词:
动脉粥样硬化; 诱导型环氧合酶; 斑块; 易损性
Keywords:
atherosclerosis;  cyclooxygenase;  plaque;  vulnerability
分类号:
R543.12
DOI:
-
文献标识码:
A
摘要:
目的:探讨诱导型环氧合酶（COX-2）在兔主动脉粥样硬化(atherosclerosis,AS)组织中的表达及其与斑块易损性之间的关系。方法: 以高脂饲料喂养建立兔主AS模型,并与正常饲料组对照。喂养12周后，取兔主动脉标本,行HE及免疫组化染色,观察COX-2、基质金属蛋白酶-2（MMP-2）、Ⅰ型和Ⅲ型胶原在AS斑块组织中的表达。结果: COX-2仅见于AS斑块，正常动脉壁无表达。AS组COX-2免疫组化染色强度均显著高于正常对照组（P<0.05）。AS组Ⅰ、Ⅲ型胶原和MMP-2免疫组化染色强度均显著高于正常对照组（P<0.05），Ⅰ/Ⅲ型胶原的比例增加。结论: COX-2在兔主动脉AS斑块中的高表达可能增加斑块的易损性。
Abstract:
AIM:To evaluate the expression of COX-2 in rabbit atherosclerotic plaque and the relationship between COX-2 and plaque vulnerability. METHODS: The rabbit aortic atherosclerotic model was developed by high cholesterol feeding. Rabbit aorta specimens were measured by HE staining and immunohistochemical staining of COX-2, MMP-2 and I/III collagen. RESULTS: COX-2 was found in atherosclerotic plaques but not in healthy or nonatherosclerotic vascular walls. COX-2, MMP-2 and I/III collagen was induced in atherosclerotic plaque lesions, implicating a relationship between COX-2 and plaque vulnerability. CONCLUSION: Overexpression of COX-2 enhances rabbit atherosclerotic plaque vulnerability.

参考文献/References

[1]Naghavi M,Libby P,Falk E,et al.From vulnerable plaque to vulnerable patient:a call for new definitions and risk assessment strategies:Part II[J].Circulation,2003,108(14):1664-1672.

[2]Rose R.Atherosclerosis--an inflammatory disease[J].N Engl J Med,1999,340(2):115-126.

[3]Lafont A.Basic aspects of plaque vulnerability[J].Heart,2003,89(10):1262-1267.

[4]Cipollone F.COX-2 and Atherosclerosis[J].J Cardiovasc Pharmacol,2006,47(suppl 1):S26-S36.

[5]Cuccurullo C,Fazia ML,Mezzetti A,et al.COX-2 expression in atherosclerosis: the good,the bad or the ugly?[J].Curr Med Chem,2007,14(15):1595-1605.

[6]Gómez-Hernández A,Martín-Ventura JL,Sánchez-Galán E,et al.Overexpression of COX-2,Prostaglandin E Synthase-1 and Prostaglandin E Receptors in blood mononuclear cells and plaque of patients with carotid atherosclerosis:Regulation by nuclear factor-κB[J].Atherosclerosis,2006,187(1):139-149.

[7]Metzner J,Popp L,Marian C,et al.The effects of COX-2 selective and non-selective NSAIDs on the initiation and progression of atherosclerosis in ApoE-/- mice[J].J Mol Med,2007,85(6):623-633.

[8]龚志锦.病理组织制片和染色技术[M].上海:上海科学技术出版社,1994:67-74.

[9]倪灿荣. 免疫组织化学实验新技术及应用[M].北京:北京科学技术出版社,1993:128-135.

[10]Rouzer CA,Marnett LJ.Cyclooxygenases: structural and functional insights[J].Lipid Res,2009,50(Supplement):S29-S34.

[11]Santovito D,Mezzetti A,Cipollone F.Cyclooxygenase and prostaglandin synthases:roles in plaque stability and instability in humans[J].Curr Opin Lipidol,2009,20(5):402-408.

[12]Shiokoshi T,Ohsaki Y,Kawabe J,et al.Downregulation of nitric oxide accumu- lation by cyclooxygenase-2 induction and thromboxane A2 production in inter- leukin-1beta-stimulated rat aortic smooth muscle cells[J].J Hypertens,2002,20(3):455-461.

[13]Sun LK,Wahl P,Bilic G,et al. CD44-mediated cyclooxygenase-2 expression and thromboxane A2 production in RAW 264.7 macrophages[J].Inflamm Res,2001,50(10):496-499.

[14]Cipollone F,Cicolini G,Bucci M,et al.Cyclooxygenase and prostaglandin synthases in atherosclerosis: Recent insights and future perspectives[J].Pharmacol Ther,2008,118(2):161-180.

[15]Cipollone F,Prontera C,Pini B,et al.Overexpression of functionally coupled cyclooxygenase-2 and prostaglandin E synthase in symptomatic atherosclerotic plaques as a basis of prostaglandin E(2)-dependent plaque instability[J].Circulation,2001,104(8):921-927.

备注/Memo

备注/Memo:
收稿日期：2010-10-28.上海市卫生局科研基金项目资助(2007105) 通讯作者：樊民，教授，主要从事冠心病临床及基础研究Email:fanmin@medmail.com.cn 作者简介：李岚，主治医师，硕士Email：lilan0824@sina.com.cn
更新日期/Last Update: 2011-12-27