Oxidative stress and apoptosis in endothelial cells exposed to PM2.5 / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12): 423-427, 2017.
Article
in Chinese
| WPRIM
| ID: wpr-510782
ABSTRACT
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 .
Full text:
Available
Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Chinese Journal of Pathophysiology
Year:
2017
Type:
Article
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