基质金属蛋白酶-9及其抑制剂在COPD合并肺间质纤维化大鼠中的作用  

The effect of MMP-9 and its inhibitor(TIMP-1)

作　　者：毕丽鑫[1] 田鹏娜[1] 王岫峥[1] 王辉[1] 赵磊[1] 贺树卿 周斌[1] 

机构地区：[1]保定市第三医院肺一科,河北保定071000

出　　处：《临床肺科杂志》2012年第3期446-447,共2页Journal of Clinical Pulmonary Medicine

摘　　要：目的观察基质金属蛋白酶-9(MMP-9)及组织型蛋白酶抑制剂-1(TIMP-1)在慢阻肺继发肺间质纤维化(PIF-COPD)大鼠肺组织中的变化,评价其与PIF-COPD的病理变化及发病机制的相关性。方法雄性大鼠24只,随机分为正常对照组(1组),21天(2组)和42天(3组)模型组。以烟熏联合气管内滴注脂多糖建立PIF-COPD模型。免疫组化法检测肺组织中MMP-9及TIMP-1水平。结果 MMP-9和TIMP-1在1组有少量表达;在2和3组MMP-9为0.1970±0.0017和0.2414±0.0017;TIMP-1为0.1265±0.0018和0.2171±0.0023(与1组相比P<0.05)水平逐渐增高且与肺间质纤维化的严重程度成正相关。结论 MMP-9及TIMP-1的水平与PIF-COPD的发病机制及病程有关。Objective This study aimed to observe the chronic obstructive pulmonary disease secondary pulmonary interstitial fi- brosis （PIF-COPD） in rats, and discuss the pathological changes and pathogenesis of correlation of PIF-COPD, through detecting the levels of MMP-9 and TIMP-1. Methods Twenty-four male rats were randomly divided into normal control group（ group 1 ） ,21 days model group （group 2 ） ,42 days model group（ group 3 ）. PIF-COPD was induced by cigarette smoke and LPS in rats. The levels of MMP-9 and TIMP- 1 in lungs were detected by immunohistochemistry. Result The MMP-9 and TIMP-1 in lung tissue of group 1 were a few expression, groups 2 and 3 were much more than group 1, and there were significant difference in groups. Conclusion The levels of MMP-9 and TIMP-1 in lung tissue of PIF-COPD may be related with disease pathogenesis, with the aggravation of MMP-9 and TIMP-1 increased gradually trend.

关 键 词：慢性阻塞性肺疾病继发肺间质纤维化 基质金属蛋白酶-9 蛋白酶抑制剂-1 

分 类 号：R563.9[医药卫生—呼吸系统]