Ferroptosis?associated cholesterol metabolism regulated by p85? in human bronchial epithelial cells with smoking

Background Chronic obstructive pulmonary disease (COPD) is characterized by inflammation, airflow obstruction, and lung damage resulting from multiple causes, in particular the exposure to cigarette smoke. Growing evidence supports an important role for lipid metabolism development of COPD, where ferroptosis plays a critical cholesterol homeostasis. The aim present study was investigate smoke extract (CSE) induction formation its potential relation with intracellular accumulation. Methods Filipin III staining content assay kit were used detect level. BODIPY C11 581/591 malondialdehyde (MDA) perioxidation. Quantitative RT-PCR mRNA level ferroptosis-related cholesterol-related genes. protein expression phosphatidylinositol 3-kinase (PI3K) signaling pathway related proteins analyzed Western blot. Results We found that CSE exogenous induced ferroptosis, while agonist increased levels. inhibition activated efflux synthesis. also regulatory roles PI3K/AKT pathway, especially p85?, ferroptosis. Conclusions CSE-induced human bronchial epithelia changed interaction between may play COPD.