中文摘要：

目的了解基质金属蛋白酶9（MMP-9）与p38丝裂原激活蛋白激酶（p38M APK）在气道粘液高分泌中的调控作用。方法利用小鼠吸入丙烯醛（21天）构建气道粘液高分泌模型,对照组采用生理盐水吸入,干预组予p38MAPK特异性抑制剂SB 203580腹腔注射。应用A日-PA S、1mmUnOhistOchemist叮、RT-PCR和W estefri-b,ot等方法,于第7天、第21天时间点取标本检测。结果丙烯醛可致小鼠出现明显的气道粘液高分泌表现,拮抗p38M APK后气道粘液物质减少、MUC 5AC和MMP-9蛋白、mRNA表达量下降。结论p38M APK信号通路特异抑制剂可减轻气道粘液分泌,其机制可能涉及调控MMP-9,从而下调MUC 5AC表达。

英文摘要：

Objective To study the effect of p38 mitogen-activated protein kinases （MAPK） and matrix metalloproteinases （MMP）-9 signaling pathway on airway mucus hyperseeretion. Methods Mice were inhaled aerolein for 21 days to set up the model of airway mucus hyperseeretion. At the same time, mice exposed aerolein were given S8203580, a p38 MAPK special inhibitor intraperitoneally during the entire experimental time, while mice in control group were received normal saline only. Animals were killed in order to reveal airway mucus overproduction by the methods of AB-PAS, immunohistoehemistry, RT-PCR and Western-blot on days 7 and 21. Results Aerolein resulted in a notable a way mucus overproduction and in turn mueosubstanee. MUCSAC, MMP-9 protein and mRNAwas decreased after SB203580 administration. Conclusion This study suggests that mucus overproduction in murine airway induced by aerolein can be ameliorated via blocking p38 MAPK signaling pathway, in which controlling the activation of MMP-9 gene may contribute to the main mechanism of MUCSAC down-regulation.