N-乙酰半胱氨酸对慢性饮酒大鼠肺纤维化的干预作用

The Intervention of N-Acetylcysteine on the Pulmonary Fibrosis of Chronic Ethanol Ingestion in Rats

目的:探讨N-乙酰半胱氨酸(NAC)对慢性饮酒大鼠肺组织的病理形态及肺组织超氧化物歧化酶(SOD)、丙二醛(MDA)含量的影响。方法:30只健康雄性大鼠随机分成乙醇组、NAC组、对照组各10只,乙醇组和NAC组每日给予乙醇液体饲料,NAC组给予NAC300mg/(kg·d)。8周后处死,观察肺组织病理改变,检测肺组织中SOD、MDA的含量。结果:乙醇组肺组织可见不同程度的肺泡壁Ⅱ型上皮细胞增生及肺泡间隔炎性细胞浸润,肺泡间隔中胶原纤维沉积增多;NAC组胶原纤维沉积和炎性细胞浸润程度比乙醇组减轻。NAC组肺泡炎、纤维化评分低于乙醇组。NAC组肺组织匀浆SOD活力高于乙醇组,MDA含量低于乙醇组,差异均有统计学意义(P<0.05或P<0.01)。结论:NAC能提高慢性饮酒大鼠肺组织SOD的活力,降低MDA的含量,减轻肺组织的纤维化程度,对慢性饮酒大鼠肺纤维化有预防作用。

Objective： To explore the influence of N-acetylcysteine （NAC） on the pulmonary fibrosis induced by chronic ethanol ingestion in rats, and observe the changes of pathogenesis of pulmonary fibrosis with detecting the content of superoxide dismutase （SOD） and malondialdehyde （MDA） of lung tissue, Methods： Thirty healthy male Sprague-Dawley rats were randomly divided into alcohol group （n=10）, alcohol＋NAC group （n=10）, and control group （n=10）. Ethanol liquid diet was given to rats in alcohol group and alcohol＋NAC group. NAC 300 mg/（kg·d） was given to rats of alcohol＋NAC group. The pathological changes of lung tissue were observed after 8-week treatment. The activity of SOD and content of MDA of lung tissue were detected. Results： there were varying degree of alveolar and alveolar septal infiltration of inflammatory ceils, and more deposition of collagen fibers at intervals of alveolar in alcohol group. The similar pathological changes were found in aleohol＋NAC group, but the degree was lower than that of alcohol group. The degree of alveolitis and the degree of pulmonary fibrosis were lower in alcohol＋NAC group than those in alcohol group （P 〈 0.05 or P 〈 0.01, respectively）. The SOD activity of lung tissue was higher in alcohol ＋NAC group than that of alcohol group. The MDA content of lung tissue was lower in alcohol＋NAC group than that of alcohol group （P 〈 0.05）. Conclusion： NAC can increase the SOD activity and decrease the content of MDA of lung tissue, and restrain the oxidative stress induced by alcohol, decrease the degree of pulmonary fibrosis induced by chronic ethanol ingestion in rats.