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目的探讨依那普利在丙烯醛所致大鼠气道黏液高分泌中的作用及其分子机制。方法用丙烯醛雾化吸入制作大鼠气道黏液高分泌模型,以依那普利作为治疗措施,于造模后1、3、6周分别用AB/PAS法检测气道黏液分泌量。免疫组化、原位杂交、RT-PCR、蛋白质印迹检测NF-κB蛋白及mRNA在气道的定位与表达量。结果丙烯醛吸入后3周,气道黏液分泌显著增加,NF-κB蛋白和mRNA表达水平明显上调,6周达到高峰;而依那普利治疗可明显下调它们的表达和黏液分泌。结论依那普利能有效控制丙烯醛所致大鼠气道黏液高分泌。其分子机制可能与NF-κB减少有关。
Objective To investigate the effect of enalapril on acrolein-induced airway mucus hypersecretion in rats and its molecular mechanism. Methods A rat model of airway mucus hypersecretion was established by inhalation of acrolein. Enalapril was used as a therapeutic measure to detect airway mucus production by AB / PAS at 1, 3 and 6 weeks after model establishment. Immunohistochemistry, in situ hybridization, RT-PCR, Western blotting were used to detect the localization and expression of NF-κB protein and mRNA in airway. Results Three weeks after inhalation of acrolein, airway mucus secretion increased significantly, and the expression of NF-κB protein and mRNA increased significantly, reaching the peak at 6 weeks. However, enalapril treatment significantly decreased their expression and mucus secretion. Conclusion Enalapril can effectively control acrolein-induced airway mucus hypersecretion in rats. Its molecular mechanism may be related to the reduction of NF-κB.