Location and dynamic changes of inflammation, fibrosis, and expression levels of related genes in SiO₂-induced pulmonary fibrosis in rats <i>in vivo</i>

Abstract

Silicosis is a serious occupational disease characterized by pulmonary fibrosis, and its mechanism and progression have not been fully elucidated yet. In this study, silicosis models of rat were established by a one-time dusting method, and the rats were sacrificed after 30, 60, and 120 days (herein referred to as the 30, 60, and 120 days groups, respectively). The rats without dust exposure were used as the control. The lungs were removed to observe pathological changes using hematoxylin and eosin and Masson’s trichrome staining and transmission electron microscopy, and the degree of collagen type I and III deposition in the lung was evaluated by enzyme‐linked immunosorbent assay. The levels of malondialdehyde and superoxide dismutase were measured by spectrophotometry, and the expression levels of fibrosis-related genes (transforming growth factor beta 1, type I collagen, type III collagen) were assessed by real-time quantitative polymerase chain reaction. The results suggested that the rats in the model groups exhibited obvious collagen fibrosis and that the severity of the lung injury increased as the time after exposure to SiO2 increased. There was a significant response to lung inflammation in the model rats, especially in the 30 days group. The degree of lipid peroxidation in bronchoalveolar lavage fluid cells and lung tissues in experiment group rats significantly increased. Among the three fibrosis-related genes, transforming growth factor beta 1was elevated in both bronchoalveolar lavage fluid cells and lung tissues of the experiment group rats, while collagen type I and III were only elevated in lung tissues. Hence, we concluded that as silicosis progressed, inflammation, fibrosis, and the expression of fibrosis-related genes showed different time-dependent changes and that a number of causal relationships existed among them.

Development of Human Lung Induction Models for Air Pollutants’ Toxicity Assessment

“…This finding is consistent with the previous investigation on A549 cells, 56 yet with a much lower exposure dose in our case, potentially accounting for the loss of epithelial integrity shown in in vivo works. 54,55 Taken together, these data indicate that the organoid-based culture can be successfully applied to test the toxicity of nanoparticles, such as nano-SiO 2 , and presumably, the toxicity of chemicals.…”

The role of macrophage-derived TGF-β1 on SiO2-induced pulmonary fibrosis: A review

“…Mechanical grinding that breaks quartz crystal for production may lead to the formation of crystal surface defects and high exposure of heterogeneous silanol groups, thus significantly increasing its biological activity (Turci et al, 2016). The diameter of SiO 2 that induces silicosis usually is less than 5 µm (Xu et al, 2019; Zhang et al, 2019a). Previous studies have shown that smaller size implies greater toxicity (Kim et al, 2019).…”

Dahuang Zhechong Pills Suppress Silicosis Fibrosis Progression via p38 MAPK/TGF-β1/Smad Pathway In Vitro

“…Its pathological features include early infiltration of inflammatory cells, persistent pulmonary inflammation, excessive deposition of extracellular matrix (ECM), interstitial fibrosis, and formation of silicon nodules [ 7 ]. Though the pathogenesis and prevention of silicosis have been explored for many years, the exact and crucial pathogenesis has not been fully elucidated [ 8 , 9 ]. In terms of treatment, there are no specific targets for screening and diagnosis of silicosis in the early stage.…”