Objective To investigate the toxicity of urban PM2.5 in Guangzhou on PC-12 cells.Methods PM2.5 was collected in Guangzhou city.PC-12 cells were cultured in vitro and divided into several groups,including the control group,PM2.5 groups with different concentrations and NAC pretreated group (pretreaed with 10 μmol/mL NAC followed with 100 μg/mL PM2.5 exposure).Cells were incubated with indicated stimulator for 24 h,then cell viability was checked with cell counting Kit-8 assay,the level of intracellular ROS was labeled using H2DCFDA fluorescence probe,cell apoptosis was measured by the flow cytometry and the expression of apoptosis-related proteins,including Cytochrome C,Caspase 9,Caspase 3 and PARP,were detected by Western Blot assay.Results PM2.5 has a strong toxicity on PC-12 cells when its concentration is over 25 μg/mL.After exposure for 24 h,the cell viability was markedly decreased.The results of flow cytometry and Western blot assay showed that PM2.5 enhanced the apoptosis of PC-12 cells with the upregulatios of Cytochrome C,Caspase 9,Caspase 3 and PARP.Pretreatment with NAC could significantly diminish PM2.5-induced PC-12 cell toxicity,decreased ROS generation and apoptosis of PC-12 cells,with the down regulations of apoptosis-related proteins.Conclusion PM2.5 can cause apoptosis of PC-12 cells by inducing oxidative stress,upregulating the Cytochrome C expression and activating Caspase9/3,which may be one of the mechanisms underlying PM2.5-induced neurotoxicity.

AIM:To study the toxicity of PM2.5 in the endothelial cells by investigating the induction of reactive oxygen species (ROS) and apoptosis in EA.hy926 cells exposed to PM2.5.METHODS: The endothelial cell line EA. hy926 was cultured in vitro and exposed to PM2.5 at different concentrations for 24 h.The cell viability was measured by CCK-8 assay and the generation of intracellular ROS was stained with DCFH-DA.The cell apoptosis was analyzed by flow cy-tometry with Annexin V-FITC/PI staining, and the protein levels of cytochrome C , caspase 9 and caspase 3 was detected by Western blot.RESULTS:After the treatment with PM2.5, the viability of the EA.hy926 cells was decreased markedly and the production of ROS was increased significantly .PM2.5 exposure upregulated the expression of cytoplasm cytochrome C and activated caspase-9 and caspase-3, resulting in the increase of the cell apoptosis significantly .The ROS generation was direct-ly involved in PM2.5-mediated endothelial cell apoptosis as N-acetyl-L-cysteine pretreatment abolished both ROS production and cell apoptosis induced by PM 2.5.CONCLUSION:PM2.5 induces oxidative stress and apoptosis in the vascular endo-thelial cells, which may be one of the mechanisms that PM2.5 influences the function of cardiovascular system .