N-acetylcysteine alleviated silica-induced lung fibrosis in rats by down-regulation of ROS and mitochondrial apoptosis signaling. (March 2014)
- Record Type:
- Journal Article
- Title:
- N-acetylcysteine alleviated silica-induced lung fibrosis in rats by down-regulation of ROS and mitochondrial apoptosis signaling. (March 2014)
- Main Title:
- N-acetylcysteine alleviated silica-induced lung fibrosis in rats by down-regulation of ROS and mitochondrial apoptosis signaling
- Authors:
- Zhang, Lin
He, Yan-Ling
Li, Qing-Zhao
Hao, Xiao-Hui
Zhang, Zuo-Feng
Yuan, Ju-Xiang
Bai, Yu-Ping
Jin, Yu-Lan
Liu, Nan
Chen, Gang
Yun, Xiang
Yao, San-Qiao - Abstract:
- <abstract> <title>Abstract</title> <p>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<abstract> <title>Abstract</title> <p>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.</p> </abstract> … (more)
- Is Part Of:
- Toxicology mechanisms and methods. Volume 24:Number 3(2014)
- Journal:
- Toxicology mechanisms and methods
- Issue:
- Volume 24:Number 3(2014)
- Issue Display:
- Volume 24, Issue 3 (2014)
- Year:
- 2014
- Volume:
- 24
- Issue:
- 3
- Issue Sort Value:
- 2014-0024-0003-0000
- Page Start:
- 212
- Page End:
- 219
- Publication Date:
- 2014-03
- Subjects:
- Analytical toxicology -- Periodicals
Toxicology -- Periodicals
Toxicology -- Methodology -- Periodicals
615.907 - Journal URLs:
- http://informahealthcare.com/loi/txm ↗
http://informahealthcare.com ↗ - DOI:
- 10.3109/15376516.2013.879974 ↗
- Languages:
- English
- ISSNs:
- 1537-6516
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 8873.042050
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 3337.xml