4.7 Article

Oxidative stress, endothelial dysfunction and inflammatory response in rat heart to NO2 inhalation exposure

期刊

CHEMOSPHERE
卷 82, 期 11, 页码 1589-1596

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2010.11.055

关键词

NO2; Oxidative stress; Endothelial dysfunction; Inflammation; Apoptosis

资金

  1. National Natural Science Foundation of PR China [20607013, 20877050, 20977060]
  2. National Natural Science Foundation of Shanxi Province [2009011049-3, 2009011046, 20051043]
  3. Specialized Research Fund for the Doctoral Program of Higher Education (SRFDP) [20091401110002]
  4. Scientific Research Foundation for the Returned Overseas Chinese Scholars of Shanxi Province
  5. Program for the Top Young Academic Leaders of Higher Learning Institutions of Shanxi

向作者/读者索取更多资源

Epidemiological studies suggest that NO2 inhalation is associated with adverse effects on heart-related health, however, existing experimental data lack relevant evidences. In this study, a role for oxidative stress, endothelial dysfunction and inflammatory responses in the heart of rats treated with different concentrations of NO2 (0, 5, 10 and 20 mg m(-3)) was investigated. Mild heart pathology occurred after 7-d exposure (6 h d(-1)). Marked oxidative stress were induced as evaluated by reduction/induction of antioxidants (Cu/Zn-SOD, Mn-SOD and GPx) activity and increasing formation of MDA and PCO. Also, mRNA and protein biomarkers of vasoconstriction (ET-1, eNOS) and inflammation (INF-alpha, IL-1 beta and ICAM-1) were up-regulated, and p53 mRNA expression, bax/bcl-2 ratio and the mean number of TUNEL-positive myocytes were increased as well. All the results implicate that NO2 exerted injuries to mammals' heart, and the damage mechanisms were possibly associated with oxidative stress, endothelial dysfunction and inflammation. (C) 2010 Elsevier Ltd. All rights reserved.

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