低分子肝素对COPD模型大鼠MCP-1及CCR2表达的影响  

Effect of Low Molecular Heparin on the Expression of MCP-1 and CCR2 in COPD Rat Model

作　　者：马珂[1] 冯玫[1] 陈天狮[2] 乔爱春[1] 李丽琪[1] 

机构地区：[1]山西医学科学院山西大医院,山西太原030032 [2]山西省人民医院,山西太原030012

出　　处：《山西职工医学院学报》2013年第6期1-3,共3页Journal of Shanxi Medical College for Continuing Education

摘　　要：目的:探讨低分子肝素对慢性阻塞性肺疾病大鼠肺组织中MCP-1及CCR2表达的影响。方法:采用气道内滴入脂多糖及连续被动熏烟法建立大鼠COPD模型,干预组皮下注射低分子肝素进行干预。观察各组大鼠肺组织病理变化,分别采用ELISA及免疫组化法测定支气管肺组织MCP-1及CCR2的表达检测分析。结果:吸烟大鼠的肺组织气道上皮细胞纤毛脱落,肺泡结构紊乱、肺泡腔扩大,部分融合形成肺大泡。模型组大鼠肺组织中MCP-1及CCR2的表达均显著高于对照组,而低分子肝素干预组的表达较模型组显著降低(P<0.05)。结论:在慢性阻塞性肺疾病的气道炎症及气道重塑中MCP-1及其受体的高表达可能具有作用,低分子肝素可能通过抑制MCP-1及其受体的过度表达而减轻气道炎症及气道重塑的作用。Objective： To explore the effect of low molecular weight heparin （LMWH） on expressions of monocyte chemoattractant protein-1 （MCP-1） and CCR2 in lung tissue of rats with chronic obstructive pulmonary disease （COPD）. Methods： Rat COPD model was established by intratrachel instillation of lipopolysaccharide （LPS） twice and continuous passive smoking. Some rats were given subcutaneous injection of low molecular heparin to intervene. The pathological changes of lung tissues were observed. The expression of MCP-1 and CCR2 in bronchopulmonary tissues were detected by ELISA and immunohistochemical method. Results： Smoking rat lung airway epithelial cilia came off; alveolar structures were disorder; alveolar cavity was expanded and formed part of the fusion pulmonary bullae. MCP-1 and CCR2 levels of COPD model were significantly higher than those of control group, and those of LMWH-treated group were significantly lower than those of COPD model. Conclusion： MCP-1 may be involved in the airway inflammation and remodeling in COPD and plays an important role. LMWH relieves the inflammation and remodeling probably by restrai- ning the expressions of MCP-1 and CCR2.

关 键 词：慢性阻塞性肺疾病 单核细胞趋化蛋白-1 CCR2 肝素 低分子量 

分 类 号：R563[医药卫生—呼吸系统]