摘要
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 explore the changes of Muc5ac expression in a rat model of mucus hyperseeretion induced by acrolein. Methods The rat model of mucus hypersceretion was established by acrolein exposure. RTPCR, ISH, immunohistoehemistry and Western blot were employed to detect the mRNA and protein levels of Muc5ac in the rats airway. Results The expression of Muc5ac was detected in trachea and lung at 3 weeks post exposure （wpe） and the expression level was enhanced at 6 wpe. ISH confirmed that Muc5ac was synthesized endogenously. Conclusion The pulmonary mucus hypersecretion is associated to the increase of intrinsic Muc5ac expression in the rat airway exposure to aerolein.
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2010年第6期994-997,共4页
Journal of Sichuan University(Medical Sciences)
基金
云南省自然科学基金(No.2010ZC206)资助
