Modeling experiments on animal models of silicosis
Modeling experiments on animal models of silicosis
Silicosis is a systemic disease characterized by progressive, diffuse fibrous tissue hyperplasia of lung tissue caused by long-term inhalation of silica-containing dust (silica dust) in the production environment. Silicosis is the oldest, the most common, the fastest progressing, the most widespread and the most serious disease among pneumoconiosis. So far, the international academic community lacks a clear understanding of its formation mechanism.
Principle
The basic principle of modeling experiments in animal models of silicosis is that SiO2 dust particles are phagocytosed by lung macrophages (dust cells) after inhalation into the alveoli, and the phagocytic vesicles containing silica dust merge with lysosomes to become secondary lysosomes.
The hydroxyl groups on the surface of quartz form hydrogen bonds with the phospholipids or proteins of the lysosomal membrane, leading to the disintegration of the lysosomes of the phagocytes, and finally the cell membrane itself is destroyed, and the silica dust is released, and then phagocytosed by other macrophages, and so on and so forth.
Damaged or destroyed macrophages release "fibrogenic factors" and activate fibroblasts, leading to proliferation of collagen fibers and the formation of fibrosis.
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