论文部分内容阅读
目的探讨血管紧张素Ⅱ(AngⅡ)在丙烯醛所致大鼠气道损伤中的表达变化及其可能作用。方法用丙烯醛雾化吸入造成大鼠气道黏液高分泌,建立模拟慢性阻塞性肺疾病模型。造模后1、3、6周分别用阿辛蓝-过碘酸雪夫(AB/PAS)法检测气道黏液分泌量。免疫组化、蛋白质印迹法检测肺上皮细胞AngⅡ的表达变化。结果大鼠丙烯醛吸入后3至6周,气管和肺组织中黏液分泌均明显增加,AngⅡ表达水平明显上调,与对照组比较差异均有统计学意义(P<0.05)。结论在丙烯醛吸入气道损伤模型中,AngⅡ明显上调,提示AngⅡ在慢性阻塞性肺疾病发病机制中可能是一个关键分子。
Objective To investigate the expression of angiotensin Ⅱ (Ang Ⅱ) in airway injury induced by acrolein and its possible role. Methods Inhalation of acrolein caused airway mucus hypersecretion in rats and established a model of chronic obstructive pulmonary disease. Airway mucus secretion was measured by Alcian blue-periodic acid Schiff (AB / PAS) at 1, 3 and 6 weeks after modeling. Immunohistochemistry and Western blotting were used to detect Ang Ⅱ expression in lung epithelial cells. Results After 3 to 6 weeks of inhalation of acrolein, the mucus secretion in the trachea and lung tissues were significantly increased, and the expression of Ang Ⅱ was significantly up-regulated compared with the control group (P <0.05). Conclusions In the airway injury model induced by acrolein, Ang Ⅱ is significantly upregulated, suggesting that Ang Ⅱ may be a key molecule in the pathogenesis of chronic obstructive pulmonary disease.