PM2.5 obtained from urban areas in Beijing induces apoptosis by activating nuclear factor-kappa B

摘要

BackgroundParticulate matter (PM), which has adverse effects on citizen health, is a major air pollutant in Beijing city. PM_2.5 is an indicator of PM in urban areas and can cause serious damage to human health. Many epidemiological studies have shown that nuclear factor-kappa B (NF-κB) is involved in PM_2.5-induced cell injury, but the exact mechanisms are not well understood. MethodsThe cytotoxic effects of PM_2.5 at 25–1600?μg/ml for 24?h were determined by MTT assay in Chinese hamster ovary cells (CHO) cells. Flow cytometry was used to determine the apoptosis rate induced by PM_2.5. The destabilized enhanced green fluorescent protein (d2EGFP) green fluorescent protein reporter system was used to determine the NF-κB activity induced by PM_2.5. The expression of pro-apoptotic Bcl-2-associated death promoter (BAD) proteins induced by PM_2.5 was determined by western blotting to explore the relationship between PM_2.5 and the NF-κB signaling pathway and to determine the toxicological mechanisms of PM_2.5. ResultsPM_2.5 collected in Beijing urban districts induces cytotoxic effects in CHO cells according to MTT assay with 72.28% cell viability rates even at 200?μg/ml PM_2.5 and flow cytometry assays with 26.97% apoptosis rates at 200?μg/ml PM_2.5. PM_2.5 increases the activation levels of NF-κB, which have maintained for 24?h. 200?μg/ml PM_2.5 cause activation of NF-κB after exposure for 4?h, the activation peak appears after 13.5?h with a peak value of 25.41%. The average percentage of NF-κB activation in whole 24?h is up to 12.9% by 200?μg/ml PM_2.5. In addition, PM_2.5 decreases the expression level of the pro-apoptotic protein BAD in a concentration-dependent manner. ConclusionsPM_2.5 induces NF-κB activation, which persists for 24?h. The expression of pro-apoptotic protein BAD decreased with increased concentrations of PM_2.5. These findings suggest that PM_2.5 plays a major role in apoptosis by activating the NF-κB signaling pathway and reducing BAD protein expression.