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

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(PIFCOPD)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l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.

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

Objective This study aimed to observe the chronic obstructive pulmonary disease secondary pulmonary interstitial fibrosis(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.