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氯沙坦在损伤血管重构中的作用及其机制的探讨(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2004年第1期
页码:
23-25,28
栏目:
实验研究
出版日期:
2004-01-01

文章信息/Info

Title:
Effect of Losartan on vascular remodelling and Losartan's influence on the wall cell apoptosis after artery injury
作者:
杨彬; 成蓓; 刘承云; 张湖萍; 江凌; 陈学林
华中科技大学同济医学院协和医院综合医疗科,湖北 武汉 430022
Author(s):
YANG Bin; CHENG Bei; LIU Cheng-yun; ZHANG Hu-ping; JIANG Ling; CHEN Xue-lin
Union Hopsital, Tongji Medical College of Huazhong University of Science and Technology,Wuhan, Hubei 430022,China
关键词:
氯沙坦; 细胞凋亡; 术后再狭窄; Bcl-2蛋白族
Keywords:
Losartan; restenosis;  VSMC apoptosis; Bcl-2 protein family
分类号:
Q255
DOI:
-
文献标识码:
A
摘要:
目的:探讨氯沙坦在大鼠血管内膜剥脱术后血管重塑中的作用及其内在机制。方法:将 Wistar大鼠随机分为假手术组、氯沙坦组及单纯 PTCA组。后两组大鼠行胸主动脉球囊损伤术,术后不同时间段处死。对主动脉的组织切片分别进行 HE染色及计算机图像分析、Tunel标记检测细胞凋亡率、免疫组化方法检测血管壁凋亡相关基因表达物 Fas、Fas-L、Bcl-2、Bax的变化。结果:单纯PTCA组术后 7、14d管壁面积明显增加,与假手术组比较有显著性差异(P<0.05)。术后14d,氯沙坦组与单纯 PTCA组比较,管壁增生程度较轻。术后7d,管壁面积增生比与细胞凋亡率之间有负相关性(r=-0.586,P<0.05),氯沙坦组的细胞凋亡率显著高于单纯PTCA组。氯沙坦组与单纯PTCA组比较,术后 7d管壁组织内Fas-L表达增加,Bcl-2表达降低(P<0.05)。结论:AT1受体拮抗剂氯沙坦可有效防止大鼠动脉损伤后的血管增生性重塑。其机制可能与促进 Fas的表达、抑制 Bcl-2的表达,从而增加细胞凋亡率有关。
Abstract:
AIM:To examine the effect of Losartan on vascular remodelling afterarter inury and the relation of Losartan to apoptosis-related gene expression on the rat models of balloon injury. METHODS: Male Wistar rats were randomzed to a standard diet or a diet supplemented with Losartan 20 mg/kg.d. The animals were sacriiced 2,7 and 14 days after the injury for examinatin of the vessel wall areas, apoptosis and the expression of Bcl-2, Ba, Fas, Fas-L in the vessel wall. RESULTS: 7 days and 14 days after anigioplasty in the PTCA group, the vessel wall areas were significantly increased as compared with the sham group.14 days after anigioplasty in the Losartan group there was a significant decrease in vessel wall areas as compared with the PTCA group. The increase in apoptosis was associated with-2 displayed an increase and a decrease respectively in Losartan animals compared with the PTCA. CONCLUSION: Losartan inhibited artery wall remodelling in the rat model of artery inury by mechanisms involving increase in Fas-L ecpression and decrease in Bcl-2 expression of which both contribyted to VSMC apoptosis.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2002-12-15
更新日期/Last Update: 2004-01-01