摘要
【目的】探讨血管紧张素Ⅱ(AngⅡ)与转化生长因子(TGF-β1)在哮喘大鼠发病中的作用,及血管紧张素受体拮抗剂(AT1)对其影响。【方法】SD清洁级大鼠40只,随机分为正常对照组(A)、卵蛋白(OVA)激发3d组(B)、OVA激发2周组(C)、OVA激发4周组(D)、OVA激发4周后AT1干预组(E)。观察各组大鼠气道结构的病理变化,OVA不同时间激发后,TGF-β1、AngⅡ在哮喘大鼠气道中的表达变化和意义及AT1对其的影响。【结果】哮喘大鼠气道随着OVA激发时间的增加而逐渐发生纤维化,AT1干预后气道纤维化有改善;AngⅡ、TGF-β1表达随OVA激发时间的延长而持续增加。应用AT1后,AngⅡ、TGF-β1表达明显低于D组(P<0.05)。【结论】①AngⅡ、TGF-β1随着气道重塑的病理改变,表达逐渐增加,说明二者对哮喘大鼠的气道重塑有促进作用;②AT1可改善气道重塑过程,可能是通过抑制气道AngⅡ、TGF-β1表达水平达到抗纤维化的作用。
[Objective] To study the effect of angiotensin Ⅱ （Ang Ⅱ ）, transforming growth factor-β1 （TGF-β1）on the development of asthmatic rats,and the influence of angiotensin Ⅱ receptor antagonist（ AT1 ）. [Methods] 40 rats were randomly divided into five groups： （A） control group,（B） challenged by OVA for 3 days, （C） challenged by OVA for 2 weeks, （D） challenged by OVA for 4 weeks, （E）using AT1 after challenged by OVA for 4weeks, and each group contains 8 rats. Study the pathologic changing of airway; the expression and significance of Ang Ⅱ and TGF-β1 and the influence of AT1 by immunohistochemical staining. [Results] The airway became fibrotic with challenged by OVA as time prolong; the intervention of AT1 could improve the fibrotic change. The expression of Ang Ⅱ and TGF-β1 became higer and higher with the challenged time prolong; the C and D groups had significant difference compared with control group（P〈0. 05）; the expression of Ang lI and TGF-β1 in E group drops significantly compared with those of group D （P〈0.05）. [Conclusion]① the expression of Ang Ⅱand TGF-β1 Ang Ⅱ gradually increase with the development of airway remodeling , which indicate they can contribuate to airway remodeling of asthmatic rats, ② AT1 can improve airway remodeling via reducing the expression of Ang Ⅱ and TGF-β1 and preventing the fibrotic changes of airway tissue.
出处
《中国儿童保健杂志》
CAS
2008年第2期188-191,共4页
Chinese Journal of Child Health Care
