摘要目的 探讨血管紧张素Ⅱ1型受体(aongiotensinⅡtype 1 receptor,AT1R)、AT2R和内素素1(endothelin-1,ET-1)在SD大鼠气道重塑模型中的表达,及糖皮质激素对其表达的影响.方法 清洁级SD大鼠,按照随机数字将其分为3组:支气管哮喘(简称哮喘)组、对照组和地塞米松干预组.建立大鼠哮喘模型,采用免疫组织化学技术结合计算机病理图像分析系统,测定大鼠气道支气管壁的ET-1、AT1R和AT2R染色的IOD值.测定完整的支气管横断面的基底膜周经和管壁面积,计算气道壁厚度.结果 哮喘组大鼠支气管壁的AT1R和ET-1表达明显高于对照组(P<0.01),地塞米松干预组大鼠的表达明显低于哮喘组(P<0.01),哮喘组、对照组和地塞米松干预组的AT2R表达有差别,但差异无统计学意义;哮喘组大鼠支气管壁ET-1和AT1R的表达均与气道壁厚度呈正相关(P<0.01),AT2R的表达与气道壁厚度无相关性;哮喘组大鼠支气管壁ET-1和AT1R的表达呈正相关(P<0.01).结论 血管紧张素Ⅱ主要通过AT1R参与了SD大鼠哮喘气道重塑过程;ET-1参与了SD大鼠哮喘气道重塑过程;糖皮质激素可通过抑制AT1R和ET-1的表达,干预气道重塑的形成;在SD大鼠哮喘气道重塑过程中ET-1和血管紧张素Ⅱ可能存在协同作用.

abstractsObjective To explore the expression of endothelin-1 (ET-1), angiotensin Ⅱ type 1 receptor(AT1R) and AT2R on the airway remodeling of asthmatic rats, and to evaluate the effects of glucocorticoid on them. Methods Healthy male SD rats were randomly divided into three groups: model group,normal group and dexamethasone group. Then, the asthmatic SD rat models were developed for investigating airway remodeling and the thickness of airway wall. The above specimens were stained by immunohistochemistry techniques for detecting ET-1, AT1R and AT2R. Histomorphometric study was done to measiure the IOD value of pulmonary bronchial walls via the staining of ET-1, AT1R, AT2R and the thickness of airway wall. Results The IOD values of pulmonary bronchial walls obtained from via the staining of ET-1 and AT1R in model group were higher than those in normal group (P = 0. 000), and higher than those in dexamethasone group (P<0.01). The expression of AT2R was differential between groups but the difference was not statistically significant. The expression of ET-1 and AT1R had positive correlation with the thickness of airway wall (P<0.01), while AT2R had no correlation with it. Conclusions Angiotensin Ⅱ mainly through AT1R, instead of AT2R involvs in airway remodeling process, ET-1 participates in the process of airway remodeling. And the expressions of ET-1 and AT1R can be inhibited by glueocortieoid. There may be synergies between ET-1 and angiotensin Ⅱ in airway remodeling process.