hsa_circ_0008500 regulates Benzo(a)pyrene-loaded gypsum-induced inflammation and apoptosis in human bronchial epithelial cells via activation of Ahr/C-myc pathways

Polycyclic aromatic hydrocarbons (PAHs) are major organic pollutants attached to fine particulate matter in the atmosphere. They induce lung inflammation, asthma, and other lung diseases. Exploring the toxic mechanism of PAHs on lung epithelial cells may provide a theoretical basis for the prevention and treatment of respiratory diseases induced by PAHs. In our study, 16 human bronchial epithelial (16HBE) cells were exposed to different concentrations of gypsum dust, Benzo(a)pyrene (BaP), and BaP-loaded gypsum dust for 24 hours. Gypsum dust loaded with BaP significantly increased the cytotoxicity of 16HBE cells, enhanced the production of lactate dehydrogenase (LDH), interleukin-6 (IL-6) and interleukin-8 (IL-8), induced cell apoptosis, and upregulate the expression of hsa_circ_0008500 (circ_0008500). The mechanism was studied with a BaP-loaded gypsum dust concentration of 1.25 mg/mL. StemRegenin 1 (SR1) pretreat significantly reduced the release of LDH, IL-6, and IL-8 and decreased the protein levels of Ahr、XAP2, C-myc, and p53. Second-generation sequencing indicated that circ_0008500 was highly expressed after 16HBE induced by BaP-loaded gypsum dust. Functional experiments confirmed that circ_0008500 promoted the inflammation and apoptosis of 16HBE cells induced by BaP-loaded gypsum dust by regulating the Ahr signaling pathway. Our study showed that fine particulate matter adsorption of BaP significantly increased the toxic effect of BaP on cells. By activating the Ahr/C-myc pathway, circ_0008500 promoted inflammation and apoptosis of 16HBE cells induced by BaP-loaded gypsum dust.