title: N-acetylcysteine alleviated silica-induced lung fibrosis in rats by down-regulation of ROS and mitochondrial apoptosis signaling.
abstract: 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.
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, Hebei United University , Tangshan, Hebei , China .
authors.forename: Lin
authors.initials: L
authors.lastname: Zhang
authors.forename: Yan-Ling
authors.initials: YL
authors.lastname: He
authors.forename: Qing-Zhao
authors.initials: QZ
authors.lastname: Li
authors.forename: Xiao-Hui
authors.initials: XH
authors.lastname: Hao
authors.forename: Zuo-Feng
authors.initials: ZF
authors.lastname: Zhang
authors.forename: Ju-Xiang
authors.initials: JX
authors.lastname: Yuan
authors.forename: Yu-Ping
authors.initials: YP
authors.lastname: Bai
authors.forename: Yu-Lan
authors.initials: YL
authors.lastname: Jin
authors.forename: Nan
authors.initials: N
authors.lastname: Liu
authors.forename: Gang
authors.initials: G
authors.lastname: Chen
authors.forename: Xiang
authors.initials: X
authors.lastname: Yun
authors.forename: San-Qiao
authors.initials: SQ
authors.lastname: Yao
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015536:Down-Regulation; D008168:Lung / Q000187:drug effects / Q000473:pathology; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology; D011347:Procollagen / Q000235:genetics; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000517:prevention & control*; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D012822:Silicon Dioxide / Q000633:toxicity*
chemical_list: D011347:Procollagen; D017382:Reactive Oxygen Species; D012822:Silicon Dioxide; D000111:Acetylcysteine