Suppression of thioredoxin system contributes to silica-induced oxidative stress and pulmonary fibrogenesis in rats
Silicosis is one of the most prevalent occupational lung diseases worldwide.This study aimed to investigate the possible mechanism that silica affected thioredoxin (Trx) system during the development of silicosis in vivo.Male Wistar rats were randomly divided into saline group and silica group in which rats were intratracheally instilled with a single dose of silica suspension (50mg in 1ml saline/rat).After 7, 15 or 30 day observation, rats were sacrificed.Biochemical parameters and histopathology were assessed.Our results demonstrated that silica could significantly cause the accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as activate antioxidative protein Nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream protein Trx in the early exposure to silica.The inhibition of Trx activity and the down-regulated expression of thioredoxin reductase (TrxR), suggesting that the function of Trx system may be suppressive induced by silica Content of lung hydroxyproline and histopathological results showed significant fibrosis development with time.In conclusion, our study demonstrated that silica could suppress the Trx system to perturb the redox balance, elicit oxidative stress, and eventually induce pulmonary fibrosis.
Thioredoxin reductase Thioredoxin Silica Pulmonary fibrosis
Zhonghui Zhu Gengxia Yang Yan Wang Jing Yang Ai Gao Piye Niu Lin Tian
Department of Occupational and Environmental Health, School of Public Health, Capital Medical University,Beijing 100069, China
国内会议
北京
英文
24-38
2014-06-01（万方平台首次上网日期，不代表论文的发表时间）