Expression of Peroxiredoxins and Pulmonary Surfactant Protein A Induced by Silica in Rat Lung Tissue.
- Author:
Nan LIU
1
;
Ling XUE
1
;
Yi GUAN
1
;
Qing Zhao LI
1
;
Fu Yuan CAO
1
;
Shu Lan PANG
1
;
Wei Jun GUAN
1
Author Information
1. School of Public Health, North China University of Science and Technology, Hebei province coal mine health and safety laboratory, Tangshan 063000, Hebei, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Disease Models, Animal;
Humans;
Lung;
enzymology;
metabolism;
Male;
Oxidative Stress;
Peroxiredoxin VI;
genetics;
metabolism;
Peroxiredoxins;
genetics;
metabolism;
Pulmonary Surfactant-Associated Protein A;
genetics;
metabolism;
Rats;
Silicon Dioxide;
toxicity;
Silicosis;
genetics;
metabolism
- From:
Biomedical and Environmental Sciences
2016;29(8):584-588
- CountryChina
- Language:English
-
Abstract:
Silicosis is one of the most serious occupational diseases in China and dates back to centuries ago. In this study, we successfully established a rat model of silicosis by intratracheal silica injection for 28 days and determined hydroxyproline levels to evaluate collagen metabolism in lung homogenates. Oxidative stress status was evaluated by detecting catalase and glutathione peroxidase activities. Expression levels of peroxiredoxins (Prx I and Prx VI) were detected by Western blotting. Pulmonary surfactant protein A (SP-A) levels in rat serum and lung tissue were analyzed by ELISA, and SP-A and Prx expression levels in lung tissues were detected by immunohistochemistry. The results suggest that Prx proteins may be involved in pulmonary fibrosis induced by silica. Downregulation of SP-A expression caused due to silica is an important factor in the occurrence and development of silicosis.
