The Protective Effect of Inhibition of PARP-1 on Inflammation Induced by PM2.5 in Human Bronchial

Objective To explore whether the inhibition of poly ADP-ribose polymerase-1(PARP-1) could attenuated inflammation induced by fine particulate matter (PM2.5) in human bronchial epithelial cell line. Methods Cell viability was detected by Trypan Blue assay after incubated with PM2.5 for 24 h. PM2.5 doses no more than 600 μg/mL were utilized in the following experiments. In order to observe how PARP-1 would effect the expression of nuclear factor-κB p65 and inducible nitric oxide synthase (iNOS), cells were respectively treated with 600 μg/mL PM2.5, 10 μmol/L 4-amino-1,8-naphthalimide (4-AN), 600 μg/mL PM2.5+10 μmol/L 4-AN or DMSO. Western blot assay was used to estimate the protein expression of PARP-1, p65 in nuclear and iNOS in cytoplasm. Nitric acid enzyme reduction assay was used to determine the production of nitric oxide (NO). Results As the PM2.5 concentration increased, the cell viability decreased, while the expression of PARP-1, p65, iNOS and NO increased significantly (P<0.05). After pretreatment of 4-AN for 24 h, the expression of PARP-1, p65, iNOS and NO almost decreased to the normal level (P>0.05). Conclusion Inflammation triggered by PM2.5 could be attenuated by the inhibition of PAPR-1, which involved the block of transcriptional activity of NF-κB for inflammatory mediator.