矽肺
乙酰半胱氨酸
细胞凋亡
肺纤维化
活性氧
纤维化
细胞色素c
药理学
化学
线粒体
肺
免疫学
内科学
内分泌学
医学
病理
生物化学
抗氧化剂
作者
Lin Zhang,Yanling He,Qingzhao Li,Xiaohui Hao,Zuo‐Feng Zhang,Juxiang Yuan,Yuping Bai,Yulan Jin,Nan Liu,Gang Chen,Yun Xiang,Sanqiao Yao
标识
DOI:10.3109/15376516.2013.879974
摘要
Reactive oxygen species (ROS) is a normal metabolic product of cellular respiration, but too much ROS can induce cell apoptosis. Here, we used N-acetylcysteine (NAC) to inhibit ROS activity to explore the effects of NAC on silica-induced pulmonary fibrosis in rats and provide evidence for study on the mechanism of silicosis. 24 adult male Sprague–Dawley rats weighing 180–220 g were randomly divided into three groups with eight rats in each group. Silicosis model group and NAC group were adopted non-tracheal exposure method of disposable intrapulmonary injection of 50 g/L, silica suspension 1 mL to establish animal silicosis model, NAC group treated with 600 mg/kg NAC by gavage from the right day of modeling, all animals were sacrificed after 28 days. The level of ROS contents and mitochondrial transmembrane potential changes of AM, the mRNA expression level of type I and type III procollagen, cytochrome C, cysteinyl aspartate specific protease-9 and caspase-3 were detected. The severity of pathological changes and pulmonary fibrosis were observed by pathologic specimens. It was showed that ROS contents and MTP changes were lower in the NAC group compared with the silicosis model group, other indexes were lower in the NAC group than the model group, but higher than those of the control group, the degree of lung fibrotic lesions observed from the pathological slices showed the same trend. These data indicated that NAC can reduce ROS content of AM in silica exposure rats, the mitochondrial apoptosis pathway can also be inhibited, the severity of pulmonary fibrosis alleviated as a result.
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