摘要
①目的 探讨建立一种由免疫复合物 (IC)介导模拟特发性肺间质纤维化病变动物模型。②方法Wistar大鼠随机分为 3组 ,分别经气管内一次性注入生理盐水 (N组 )、博莱霉素 (B组 )、免疫复合物 (I组 )。第 7、1 4、2 8天处死动物 ,利用生化和组织病理等方法比较各组肺系数、羟脯氨酸 (HyP)含量及肺泡炎、纤维化的程度。③结果 第 7、1 4、2 8天时 ,I组肺组织肺系数均显著低于B组 (F =8.4 88～ 1 3.0 95 ,q =4 .0 5 2～ 5 .376 ,P <0 .0 5 ) ,与N组相比 ,差异无显著性 (q =1 .2 89～ 1 .739,P >0 .0 5 )。I组羟脯氨酸含量与N组相比差异显著 (F =1 7.6 91～31 .85 8,q =6 .5 83～ 1 0 .71 9,P <0 .0 5 )。I组肺泡炎及纤维化程度均较N组重 (F =6 .6 82～ 33.2 5 0 ,q =4 .2 84～7.5 92 ,P <0 .0 5 ) ,但轻于同期B组水平 (q =3.5 70～ 5 .1 1 6 ,P <0 .0 5 )。④结论 可以通过免疫复合物的介导建立肺间质纤维化模型。
Objective To study an idiopathic pulmonary fibrosis(IPF) model mediated by immuno-complex(IC). Methods Experimental Wistar rats were randomly divided into three groups: groups N, B, and I. Intratracheal injection of normal saline, bleomycin, and IC was done respectively for each group. The rats were killed on day 7, 14,and 28. Lung co-efficient, hydroxyproline, severity of alveolitis and fibrosis were compared between them by biochemical and pathological methods. Results Lung co-efficient and hydroxyproline in group I were significantly different from those in group B( F=8.488-13.095,q=4.052-5.376,P <0.05). The severity of alveolitis and fibrosis were also significantly increased in group I than those in group N( F= 6.682- 33.250,q=4.284-7.592,P <0.05). Conclusion An IPF model can be established by mediation of IC.
出处
《青岛大学医学院学报》
CAS
2004年第2期112-113,116,共3页
Acta Academiae Medicinae Qingdao Universitatis
