Chronic lung inflammation and pulmonary fibrosis after multiple intranasal instillation of <scp> PM ₂ </scp> _.5 in mice

Fine particulate matter (PM2.5) is an important component of air pollution and can induce lung inflammation oxidative stress. We hypothesized that PM2.5 could play a role in the induction pulmonary fibrosis. examined whether multiple intranasal instillation fibrosis mouse, also investigated underlying pro-fibrotic signaling pathways. C57/BL6 mice were intranasally instilled with 50 ?l suspension (7.8 ?g/g body weight) or PBS three times week over 3 weeks, 6 weeks 9 weeks. To observe recovery after termination exposure, week-PM2.5 studied at instillation. There significant decreases total capacity (TLC) compliance (Cchord) 9-week PM2.5-instilled mice, while there increased histological scores enhanced type I collagen hydroxyproline deposition, mitochondrial ROS levels NOX activity, decreased SOD GSH levels, accompanied by number aberrant morphology (swelling, vacuolization, cristal disruption, reduced matrix density) mice. Multiple resulted expression TGF?1, increases N-Cadherin Vimentin decrease E-Cadherin. It led to OPA1 MFN2, Parkin, SQSTM1/p62, ratio light china (LC) 3B II LC3B I, PI3k/Akt phosphorylation, NLRP3 expression. Intranasal for induced fibrosis, which was linked epithelial-mesenchymal transition, stress, damage mitophagy, as well activation TGF?1-PI3K/Akt, TGF?1- TGF?1-NLRP3