Bisphenol AP promotes the development of bleomycin-induced pulmonary fibrosis by regulating macrophage function
Bisphenol AP (BPAP), a structural analogue of bisphenol A (BPA), has been frequently detected in humans. The presence of BPAP is linked to various adverse health outcomes, including metabolic diseases and mood disorders. However, the effects by which BPAP contributes to lung diseases remain inadequately understood. This study utilized the mouse macrophage cell line RAW 264.7 and bleomycin induced pulmonary fibrosis model (PF) of C57BL/6 mice to explore the effects of BPAP. Functional experiments demonstrated that BPAP exposure inhibited macrophage proliferation and enhanced oxidative stress. Additionally, BPAP exposure enhanced the phagocytic and chemotactic functions of macrophages. Overall design: To explore the molecular mechanisms underlying the effects of BPAP on macrophages, RNA-seq was conducted to identify the differentially expressed genes (DEGs) in response to BPAP exposure.