Intratracheal administration of polystyrene microplastics induces pulmonary fibrosis by activating oxidative stress and Wnt/β-catenin signaling pathway in mice.

Polystyrene microplastics (PS-MPs) are emerging pollutants that are absorbed by organisms. Due to their small volume and strong biological permeability, they affect the biological functions of cells. In recent years, several studies have detected PS-MPs in air samples, which may damage the human respiratory system following inhalation. The Masson trichrome staining, immunofluorescence, and western blotting assays were conducted to analyze the effects of PS-MPs on pulmonary fibrosis. Alveolar epithelial injuries were assessed through confocal microscopy, and the levels of SOD and GSH were used to evaluate oxidative stress. Our analyzes demonstrated that inhalation of the PS-MPs induces pulmonary fibrosis in a dose-dependent manner in mice. In high dose group (6.25 mg/kg), the PS-MPs significantly increased the expression of α-SMA, Vimentin and Col1a (p < 0.05). Immunofluorescence assays showed decreased levels of SP-C and increased levels of KL-6 in the PS-MPs group. The suppression of SOD (1.46 times) and GSH-Px (2.27 times) indicated that inhalation of microplastics triggered intensive oxidative stress in lungs. Moreover, there was activation of the Wnt/β-catenin signaling pathway in the PS-MPs group. In addition, the data showed that antioxidant melatonin (50 mg/kg) alleviated the PS-MPs-induced pulmonary fibrosis. Taken together, our analysis demonstrated that inhalation of polystyrene microplastics induces pulmonary fibrosis via activation of oxidative stress and Wnt/β-catenin signaling pathway in mice.