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[诱导型一氧化氮合酶在再狭窄大鼠中的表达及黄芪和当归的作用]

[Expression of inducible nitric oxide synthase in restenosis rats and function of Astragalus membranaceus and Angelica sinensis].

作者信息

Yang Changchun, Ma Zengchun

机构信息

General Hospital of Chinese People's Armed Police Forces, Beijing 100039, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2012 Jun;37(11):1655-8.

PMID:22994002
Abstract

OBJECTIVE

To explore the expression of inducible nitric oxide synthase (iNOS) in restenosis rats and function of Astragalus membranaceus and Angelica sinensis.

METHOD

The restenosis model was established by denuding aorta endothelium, rats were randomly divided into control group, model group, A. membranaceus treatment group, A. sinensis treatment group, combined A. membranaceus with A. sinensis treatment group. After intramuscular injection of drugs for 21 dayss, the changes of iNOS in restenosis rats were observed by histomorphology and immunohistochemisty, the effects of A. membranaceus and A. sinensis on iNOS in restenosis rats was also investigated.

RESULT

A small quantity of iNOS were detected in the intima and media of normal aorta, the expression of iNOS was increased on 3 day after denuding aorta endothelium, the expression of iNOS increasd and the color darken along with injury damage and intima thickening. Compared with model group, the expression of iNOS decreasd in A. membranaceus, A. sinensis treated group, A. membranaceus and A. sinensis treated group changed more significantly.

CONCLUSION

iNOS was involved in blood vessel restenosis by denuding aorta endothelium, A. membranaceus, A. sinensis could inhibit intimal proliferation through iNOS.

摘要

目的

探讨诱导型一氧化氮合酶(iNOS)在血管再狭窄大鼠中的表达以及黄芪和当归的作用。

方法

通过剥脱大鼠主动脉内皮建立血管再狭窄模型,将大鼠随机分为对照组、模型组、黄芪治疗组、当归治疗组、黄芪与当归联合治疗组。肌肉注射药物21天后,采用组织形态学和免疫组织化学方法观察血管再狭窄大鼠iNOS的变化,研究黄芪和当归对血管再狭窄大鼠iNOS的影响。

结果

正常主动脉内膜和中膜可检测到少量iNOS,剥脱主动脉内皮后3天iNOS表达增加,随着损伤加重和内膜增厚,iNOS表达增加且颜色加深。与模型组相比,黄芪治疗组、当归治疗组、黄芪与当归联合治疗组iNOS表达均降低,联合治疗组变化更明显。

结论

iNOS参与了剥脱主动脉内皮所致的血管再狭窄,黄芪、当归可通过抑制iNOS表达抑制内膜增殖。

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Zhongguo Zhong Yao Za Zhi. 2012 Jun;37(11):1655-8.
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