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奥美沙坦对大鼠移植静脉内膜重构过程中整合素β-3/FAK信号蛋白表达的影响

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第2期
页码:
164-167
栏目:
基础研究
出版日期:
2010-03-04

文章信息/Info

Title:
Expression of integrin β-3/focal adhesion kinase on intimal remodeling of rat vein graft: modulation by olmesartan
作者:
肖平喜1田乃亮1葛震1张娟1裴兆辉2王礼春2马虹2
1.南京医科大学附属南京第一医院心内科,江苏 南京 210006;2.中山大学附属第一医院心内科,广东 广州 510080
Author(s):
XIAO Ping-xi1 TIAN Nai-liang1 GE Zhen1 ZHANG Juan1 PEI Zhao-hui2 WANG Li-chun2 MA Hong2
1.Department of Cardiology, Nanjing First Hospital Affiliated Nanjing Medical University, Nanjing 210006, Jiangsu, China; 2.First Affiliated Hospital, SUN YAT-sen University, Guangzhou 510080, Guangdong, China
关键词:
奥美沙坦重构黏着斑激酶
Keywords:
olmesartan remodeling focal adhesion kinase
分类号:
R972
DOI:
-
文献标识码:
A
摘要:
目的: 观察奥美沙坦对大鼠移植静脉内膜重构过程中整合素β-3(integrinβ-3)黏着斑激酶(focal adhesion kinase,FAK)表达的影响。方法: 建立大鼠移植静脉桥模型,将36只雄性SD大鼠被随机分成模型对照组、奥美沙坦组及生理盐水对照组,每组12只。取移植静脉切片、HE染色观察各组血管壁内膜的厚度。采用免疫组化染色法观察各组血管平滑肌细胞(SMC)增殖核抗原(PCNA)的表达。采用Western blot法检测整合素β-3和FAK的表达。结果: 与模型对照组相比,奥美沙坦组内膜的厚度明显减轻(P<0.05);PCNA和FAK的表达明显降低(P<0.05)。生理盐水对照组与模型对照组相比,内膜的厚度无明显减轻;PCNA和FAK的表达无明显改变。结论: 大鼠移植静脉内膜重构过程中,伴随整合素β-3/FAK信号蛋白的表达,奥美沙坦可抑制大鼠移植静脉内膜重构,此作用可能与下调FAK信号蛋白的表达有关。
Abstract:
AIM: To observe the expression of focal adhesion kinase in rat’s autologous vein graft and its modulating effect by olmesartan (a specific type 1 angiotensin II receptor antagonist). METHODS: Autologous external jugular veins were grafted to common carotid arteries in 36 male Wistar rats. After surgery, rats were randomly assigned to three groups (12 rats in each): model control group, olmesartan group and physiological saline group. The intimal thickness in vein grafts was quantitated in H/E-stained segments. Integrin β-3 and focal adhesion kinase expression levels were assessed by Western blotting, and proliferating cell nuclear antigen (PCNA) was measured by immunohistochemistry. RESULTS: Neointimal hyperplasia was observed in model control group characterized by significant intimal thickening. The expressions of integrin β-3, FAK and PCNA were positive in model control group. Compared with that in model control group, the intimal thickness was significantly attenuated in olmesartan group (P<0.05) and the expressions of FAK and PCNA significantly reduced (P<0.05). CONCLUSION: FAK is involved in the restenosis of vein graft in rats. Olmesartan attenuates the restenosis of rat vein graft, possibly through its downregulating effect on FAK.

参考文献/References

[1] 兰锡纯,冯卓荣. 心脏血管外科学[M]. 北京: 人民卫生出版社, 2002:859-962.

[2] Yoshida Y, Mitsumata M, Ling G, et al. Migration of medial smooth muscle cells to the intima after balloon injury[J]. Ann N Y Acad Sci, 1997, 8(11):459-470.

[3] 温进坤,韩梅,程云会,等. 整合素β-3-粘着斑激酶信号途径的活化参与大鼠血管新生内膜的形成[J]. 中国病理生理杂志, 2006, 22(10):1922-1925.

[4] Yau JM, Alexander JH, Hafley G, et al. Impact of perioperative myocardial infarction on angiographic and clinical outcomes following coronary artery bypass grafting (from PRoject of ex-vivo Vein graft ENgineering via Transfection[J]. Am J Cardiol, 2008, 102(5):546-551.

[5] Mehta PK, Griendling KK. Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system[J]. Am J Physiol Cell Physiol, 2007, 292(1):C82-C97.

[6] Furubayashi K, Takai S, Jin D, et al. The significance of chymase in the progression of abdominal aortic aneurysms in dogs[J]. Hypertens Res, 2007, 30(4):349-357.

[7] Govindarajan G, Eble DM, Lucchesi PA, et al. Focal adhesion kinase is involved in angiotensin II-mediated protein synthesis in cultured vascular smooth muscle cells[J]. Circulation Res, 2000, 87(8):710-716.

[8] Zannad F, Fay R. Blood pressure-lowering efficacy of olmesartan relative to other angiotensin II receptor antagonists: an overview of randomized controlled studies[J]. Fundam Clin Pharmacol, 2007, 21(2):181-190.

[9] Mizuno M, SadaT, Ikeda M, et al. Pharmacology of CS-866, a novel nonpeptide angiotensinⅡ receptor antagonist[J]. Eur J Pharmacol, 1995, 285(2):181-188.

[10]Koike H, Sada T, Mizuno M. In vitro and in vivo pharmacology of olmesartan medoxomil, an angiotensin Ⅱ type AT1receptor antagonist[J]. J Hypertens Suppl, 2001, 19(1):S3-S14.

[11]Warner GT, Jarvis B. Olmesartan medoxomil[J]. Drugs, 2002, 62(9):1345-1353.

[12]Li S, Wang X, Qiu J, et al. Angiotensin II stimulates endothelial integrin beta3 expression via nuclear factor-kappaB activation[J]. Exp Aging Res, 2006, 32(1):47-60.

[13]Li X, Lee JW, Graves LM, et al. Angiotensin II stimulates ERK via two pathways in epithet- lial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway[J]. EMBO J, 1998, 17(9):2574-2583.

备注/Memo

备注/Memo:
收稿日期:2009-3-29.通讯作者:裴兆辉,副主任医师,主要从事心血管临床与基础研究Email:leak123@126.com作者简介:肖平喜,医师,博士Email:sysu-xiao@163.com
更新日期/Last Update: 2010-03-05