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作 者:陈霞[1] 佟丽[1] 程兆忠[1] 韩伟忠[1] 李斌[2]
机构地区:[1]青岛大学医学院附属医院呼吸内科,山东青岛266003 [2]潍坊市人民医院急诊内科
出 处:《青岛大学医学院学报》2010年第4期322-325,共4页Acta Academiae Medicinae Qingdao Universitatis
基 金:青岛市科技局计划课题(06-2-2-3-nsh-5)
摘 要:目的观察低分子肝素(LMWH)对慢性阻塞性肺疾病(COPD)大鼠模型肺组织细胞间黏附分子-1(ICAM-1)和单核细胞趋化蛋白-1(MCP-1)表达的影响。方法将Wistar大鼠30只随机分为正常对照组、COPD模型组、LMWH干预组,每组10只。采用熏吸香烟加气管内注入脂多糖的方法建立COPD模型,LMWH干预组于COPD模型开始建立时皮下注射LMWH 150 U/kg,每天1次。观察各组肺组织病理改变、血气指标、肺泡灌洗液(BALF)的细胞计数及分类,应用免疫组化法测定肺组织ICAM-1、MCP-1的表达情况。结果所建COPD模型的病理学改变符合人类COPD的特点。与COPD模型组比较,LMWH干预组肺组织的病理改变轻,BALF中白细胞总数、中性粒细胞数百分比明显下降(F=146.77、106.63,q=10.29、12.42,P<0.01),肺组织ICAM-1、MCP-1的表达明显减弱(F=32.08、56.36,q=6.87、8.68,P<0.01)。结论ICAM-1和MCP-1参与了气道炎症的发生,LMWH可能通过抑制ICAM-1、MCP-1表达而减轻COPD气道炎症。Objective To observe the effect of low molecular weight heparin(LMWH) on expressions of intercellular adhesion molecular-1(ICAM-1) and monocyte chemoattractant protein-1(MCP-1) in lung tissue of rats with chronic obstructive pulmonary disease(COPD). Methods Thirty Wistar rats were equally randomized to three groups;control group,COPD-model group and LMWH-treated group.A COPD model was created by intratracheal instillation of lipopolysaccharide and exposed to cigarette smoking.Hypodermic injection of LMWH,150 U/kg once a day,was offered to the rats in LMWH group,starting from the day upon completion of the model.Pathologic changes of the lung tissue,blood gas and the total and differential cell counts of bronchoalveolar lavage fluid in all three groups were determined.The expressions of ICAM-1 and MCP-1 were observed immunohistochemically. Results The pathological changes in the COPD model were coincident with that in human.Compared with COPD-model group,pathological changes of the lung tissue in LMWH-treated group were milder,the total white blood cells and the percentage of neutrophils in BALF decreased(F=146.77,106.63;q=10.29,12.42;P0.01),the expressions of ICAM-1 and MCP-1 decreased(F=32.08,56.36;q=6.87,8.68;P0.01) Conclusion ICAM-1 and MCP-1 involve in the process of airway inflammation,and LMWH relieves the inflammation probably by restraining the expressions of ICAM-1 and MCP-1.
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