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 days instillation, 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.