Abstract:

Objective To investigate the expression of autophagy-related proteins LC-3 and Beclin-1 in the rat silicosis model
and its mechanisms, and to study the molecular mechanism of silicosis formation from cells autophagy perspective. Methods Ninety
healthy male SD rats were randomly divided into three groups: control group, model group and autophagy inhibitor 3-methyladenine
(3-MA) group (n=30). The rat silicosis model was made by one-time infusion of the silica dust suspension method, using the
non-exposed tracheal intubation, and was given the 3-MA. The rats were sacrificed on the 1st, 3rd, 7th, 14th and 28th day after
the modeling. The morphological changes of lung tissue were observed by HE and Masson staining.The expression of LC-3 and Beclin-1
were detected by means of immunohistochemistry and Western blotting. Results There were alveolitis change, silicosis nodules
formation and collagen deposition in the model group.The intensities of immunohistochemical positive reaction for LC-3 and Beclin-1
increased at all time points in the model group (P<0.05). LC-3 and Beclin-1 expressions began to increase at the 1st day, peaked
at the 14th day(P＜0.05), and decreased at the 28th day, but higher than basal expression. Compared with the model group, alveolitis
change, the area and number of silicotic nodules and collagen deposition decreased, and the expression of LC-3 and Beclin-1
decreased at all time points in the 3-MA group(P＜0.05). No significant changes in the trend of each point in time was observed.
Conclusion Autophagy may be involved in the pathological process of silicosis in rats, and played an important role in the
occurrence and development of silicosis.

Key words: Autophagy, Silicosis, LC-3, Beclin-1, Masson staining, Immunohistochemistry, Western blotting, Rat