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Diesel exhaust particles induced oxidative stress, autophagy, and apoptosis in human umbilical vein endothelial cells
Yang Guo1, Longfei Guan2, Yu Ji3, Hangil Lee4, Wenjing Wei5, Changya Peng6, Xiaokun Geng7, Yuchuan Ding6
1 Department of Neurology, Beijing Luhe Hospital, Capital Medical University, Beijing, China
2 Department of Neurology; China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China; Department of Neurosurgery, Wayne State University School of Medicine; Department of Research and Development Center, John D. Dingell VA Medical Center, Detroit, MI, USA
3 Department of General Surgery, Beijing Luhe Hospital, Capital Medical University, Beijing, China
4 Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA
5 Department of Neurology, China-America Institute of Neuroscience, Xuanwu Hospital, Capital Medical University, Beijing, China
6 Department of Neurosurgery, Wayne State University School of Medicine; Department of Research and Development Center, John D. Dingell VA Medical Center, Detroit, MI, USA
7 Department of Neurology; China-America Institute of Neuroscience, Beijing Luhe Hospital, Capital Medical University, Beijing, China; Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI, USA
Correspondence Address:
Dr. Xiaokun Geng
Department of Neurology, Beijing Luhe Hospital, Capital Medical University, No. 82 Xinhua South Road, Tongzhou District, Beijing 101149
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ed.ed_37_20
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Background: Air pollution is one of the greatest public health concerns worldwide. In order to understand its mechanism of harm, we investigated the effects of diesel exhaust particles (DEPs), one of the major constituents of ambient air pollutants, on reactive cell viability, oxygen stress, autophagy, and apoptosis.
Materials and Methods: In in vitro human umbilical vein endothelial cell (HUVEC) model, cells were exposed to freshly dispersed DEP preparations at 0, 12.5, 25, 50, 100, or 200 µg/mL for 24 h or at 50 µg/mL DEP for 1, 3, 6, 12, or 24 h. Cell survival and oxidative stress were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), and generation of reactive oxygen species (ROS). Protein expressions of autophagy (Beclin-1, p62, and light chain 3 [LC3]-II) and apoptosis (Bcl2 and Bax) were assayed by Western blotting.
Results: DEP induced a significant dose-dependent and temporal decrease in cell viability and increase in ROS generation and NOX activity, in association with decreased or increased protein levels of p62 or Beclin-1, as well as conversion of the LC3 in a dose-dependent manner. DEP increased pro-apoptotic protein Bax and decreased anti-apoptotic protein Bcl2.
Conclusions: These results demonstrated that DEP exposure induced cytotoxicity, oxidative stress, autophagy, and apoptosis in HUVECs. Novel insight into the mechanisms of cardiovascular diseases caused by air pollution may be provided through these findings.
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