摘要
目的了解树突状细胞表面因子OX62、CD83在慢阻肺大鼠肺部的表达变化,并探讨CCL20抗体的干预作用。方法选用30只健康Wistar大鼠,随机分为健康对照组(10只)、慢阻肺模型组(10只)、CCL20单抗组(10只),用气道内注入脂多糖(共2次)联合烟雾刺激(约28 d)的方法诱导慢阻肺模型。在实验初始对单抗组大鼠以CCL20单克隆抗体腹腔注射一次。在第29天取大鼠的肺组织观察其病理学改变,用免疫组织化学技术检测肺部树突状细胞(DC)的表面因子OX62、CD83的表达变化。结果模型组大鼠肺组织HE染色符合气道炎症和肺气肿的表现,CCL20单抗组大鼠肺部病理表现比慢阻肺组明显减轻。与健康对照组相比,慢阻肺模型组大鼠的肺组织中OX62的表达比对照组明显增多(P<0.05),而在CCL20单抗组低于慢阻肺组(P<0.05)。慢阻肺模型组大鼠肺组织中CD83的表达比对照组少(P<0.05),而在慢阻肺组与CCL20单抗组之间则没有明显的差异(P>0.05)。结论慢阻肺的发病可能与肺部OX62的表达增多及CD83的表达减少有关,使用CCL20单抗能部分地抑制这一效应。
Objective To understand the expression of OX62 and CD83 in the lungs of rats with COPD,and to investigate the effect of the CCL20 monoclonal antibody on it. Methods A total of 30 rats were randomly divided into three groups： normal,model,and CCL20 antibody treated. COPD was induced by cigarette smoke exposure 28 days and LPS solution injection twice. The rats were injected with CCL20 antibody in the last group on the first day. The rats were sacrificed on the 29 th day. We investigated the pathomorphology of their lungs by HE staining and evaluated the DC distribution in their lungs by immunohistochemistry. Results The HE staining results of the COPD models are consistent with the typical pathological features of COPD patients,the lung pathology in CCL20 group was significantly attenuated thanthat in the COPD group. Compared with healthy control group,the OX62 ＋ DCs in the COPD model group was significantly increased（ P 〈 0. 05）,and the CCL20 group was lower than that in the COPD group（ P 〈 0. 05）. The CD83 ＋ DCs of COPD group was lower than that in healthy control group（ P 〈 0. 05）,and the difference was not statistically significant between COPD and CCL20 treated group（ P 〉 0. 05）. Conclusion The pathogenesis of COPD may be related to the increase of OX62 ＋ DC and the decrease of CD83 ＋ DC,and this effect could be partly inhibited by CCL20 antibody.
出处
《中国比较医学杂志》
CAS
北大核心
2016年第3期11-14,10,共5页
Chinese Journal of Comparative Medicine
基金
国家自然科学基金(81460008)
