Silicosis is an occupational disease that seriously damages the life and health of miners. Herein, we constructed a mouse model of silicosis and used label-free confocal Raman spectroscopy to analyze… Click to show full abstract
Silicosis is an occupational disease that seriously damages the life and health of miners. Herein, we constructed a mouse model of silicosis and used label-free confocal Raman spectroscopy to analyze the biomolecular variations in lung fibrous nodules and inflammatory sites. The mice were exposed to silica particles for 1 month (SIL-1M group), 3 months (SIL-3M group), or no exposure (control tissues, NS). Raman spectra obtained from treated and untreated lung tissue were subjected to chemometric analysis to quantify biochemical composition differences in the silicosis. Simultaneously, immunohistochemistry and collagen staining were used to evaluate inflammation, fibrosis, and apoptosis. As a result, the SIL-1M and SIL-3M groups showed significant differences in cholesterol, lipids, amino acids, nucleic acids, and cytochrome C, and the collagen peaks at 1248 cm-1 and 1448 cm-1 were significantly higher than in the NS group. Notably, glycogen and phospholipid may be an inflammatory indicator consistent with NF-κB expression. In addition, significant differences in collagen and cytochrome C content in silicosis lung tissue were found using Raman spectroscopy and were verified by Masson's staining and Bax/Bcl-2 expression ratio. In summary, our findings provide a label-free technique to understand the biochemical changes in lung inflammatory and fibrosis microenvironment after exposure to silica particles and provide a valuable reference for studying the mechanism of silicosis.
               
Click one of the above tabs to view related content.