论文部分内容阅读
目的探讨内源性黏蛋白5ac(Muc5ac)在丙烯醛所致大鼠气道损伤中的表达变化及其作用机制。方法用丙烯醛雾化吸入造成大鼠气道黏液高分泌,模拟慢性阻塞性肺疾病。造模后分别用免疫组织化学、Western blot、RT-PCR和原位杂交检测气道Muc5ac的表达变化及定位分布。结果丙烯醛吸入后第1周气道中Muc5ac的基因及蛋白水平均明显上调,并继续上调至第6周达最高水平。Muc5ac表达主要分布于气管、支气管上皮及肺泡上皮细胞中。结论内源性Muc5ac在丙烯醛处理致大鼠气道黏液高分泌中明显增加,提示其在慢性阻塞性肺疾病黏液高分泌发病机制中可能是一个重要分子。
Objective To investigate the expression of endogenous mucin 5ac (Muc5ac) in acrolein-induced airway injury in rats and its possible mechanism. Methods Inhalation of acrolein caused airway mucus hypersecretion in rats and simulated chronic obstructive pulmonary disease. After modeling, immunohistochemistry, Western blot, RT-PCR and in situ hybridization were used to detect the changes of airway Muc5ac expression and localization. Results In the first week after acrolein inhalation, Muc5ac gene and protein levels were significantly increased, and continue to rise to the highest level of the sixth week. Muc5ac expression mainly in the trachea, bronchial epithelial cells and alveolar epithelial cells. Conclusion Endogenous Muc5ac is significantly increased in mucus hypersecretion of rat airway induced by acrolein, suggesting that Muc5ac may be an important molecule in the pathogenesis of mucus hypersecretion in chronic obstructive pulmonary disease.