吸入布地奈德对哮喘大鼠肺组织嗜酸粒细胞趋化因子及受体表达水平的影响

目的观察吸入布地奈德对哮喘大鼠肺组织嗜酸粒细胞趋化因子及受体表达水平的影响。方法将30只Wistar大鼠随机分组(n=10):模型组(A组)采用OVA致敏与激发;空白对照组(C组),以生理盐水代替OVA;布地奈德组(B组),第6次诱发哮喘结束后30 min采用BUD混悬液雾化吸入2周。模型组和空白对照组以等量生理盐水代替。肺组织嗜酸性粒细胞(EOS)计数,测定肺组织Eotaxin蛋白、CCR3蛋白表达水平。结果布地奈德组大鼠肺组织EOS计数明显低于模型组(8.87±3.21)vs(11.53±4.50),P0.05]。哮喘大鼠肺组织中有大量的Eotaxin蛋白、CCR3蛋白表达,布地奈德组大鼠肺组织Eotaxin蛋白、CCR3蛋白表达明显减少。空白对照组在上述部位仅少量表达或不表达。结论 Eotaxin及其受体CCR3参与哮喘的发病机制,布地奈德雾化吸入治疗哮喘与其抑制Eotaxin及其受体CCR3表达有关。

Effects of budesonide inhalation on Eotaxin,CCR3 level in lung of asthma rats

Objective To observe the effects of budesonide inhalation on Eotaxin,CCR3 level in lung of asthma rats.Methods Thirty Wistar rats wre randomly divided into three groups with 10 rats each group：the asthma group（A group,allergized and stimulated by OVA）,the budesonide group（B group,treated with budesonide inhalation）,the control group（C group,NS substituted for OVA and budesonide inhalation）.The level of Eotaxin,CCR3 were examined by Elisa Kit.Results Compared with C group,the level of Eotaxin,CCR3 in A group rats was significantly high（P0.05）.Compared with A group,the level of Eotaxin,CCR3 in B group rats was significantly low（P0.05）.EOS was statistically diminished in B group compared with A group.Conclusion Eotaxin and CCR3 were involved in asthma＇s pathophysiological process.Budesonide inhalation can attenuate asthma seizure through inhibiting the expression of Eotaxin and CCR3.