Objectives: 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).
Conclusions: 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.
Keywords: Inflammation; NF-κB; PM2.5; Poly ADP-ribose polymerase-1 (PARP-1).