【摘要】 目的:探讨布地奈德对哮喘模型鼠骨髓及肺组织中CD34+、嗜酸粒细胞趋化因子(Eotaxin)及嗜酸性粒细胞趋化因子受体(CCR3)表达的影响及其治疗哮喘的可能机制。方法:健康雄性豚鼠30只随机分成对照组(A组)、哮喘组(B组)及布地奈德治疗组(C组),每组10只。B、C组以卵白蛋白(OVA)作为抗原腹腔内注射联合雾化吸入复制哮喘模型,末次激发后6h处死豚鼠,制备豚鼠肺组织病理标本和骨髓标本,苏木精-伊红(HE)染色观察肺组织炎症改变;免疫组化检测CD34+祖细胞、Eotaxin及CCR3在肺组织中的表达。结果:哮喘组肺组织CD34+祖细胞、Eotaxin及CCR3的阳性细胞数明显增加;布地奈德治疗组肺组织中CD34+祖细胞、Eotaxin及CCR3的表达均有不同程度的减轻,与哮喘组比较,差异均有统计学意义(P<0.01)。结论:布地奈德可通过下调骨髓及肺组织中CD34+祖细胞、Eotaxin及CCR3的表达水平,发挥其抗气道炎症的作用。更多还原

【Abstract】 Objective:To explore the effect of budesonide on changes of CD34,EOTAXIN and CCR3in the lung and bone marrow of asthma guinea pig with asthma.Methods:A total of 30healthy male guinea pigs were randomly divided into control group(A),asthma group(B)and budesonide group(C). Asthma model was established in B,C group by intraperitoneally injection and inhalation of ovalbumin(OVA).Guinea pigs were executed 6hafter the last outbreak.Then guinea pig lung tissue specimens and bone marrow samples were prepared.Inflammation of lung tissue was detected by hematoxylin-eosin staining,and the expression of CD34+progenitor cells,Eotaxin and CCR3in the lung tissue were detected by immunohistochemical assay.Results:The expression of tissue CD34+progenitor cells,Eotaxin and CCR3-positive cells in asthma lung was significantly increased;while the budesonide group showed decrease trendy,and the difference were statistically significant between the two groups(P<0.01).Conclusions: Budesonide can down-regulate the expression of CD34+bone marrow progenitor cells,Eotaxin and CCR3 in the lung tissue and marrow,and plays a role in anti airway inflammation.更多还原