TY - JOUR
T1 - Particulate matter (PM 10) exposure induces endothelial dysfunction and inflammation in rat brain
AU - Guo, Lin
AU - Zhu, Na
AU - Guo, Zhen
AU - Li, Guang ke
AU - Chen, Chu
AU - Sang, Nan
AU - Yao, Qing chen
N1 - Funding Information:
This study was supported by National Natural Science Foundation of P. R. China (NSFC, No. 20607013 , 20877050 , 20977060 ), Natural Science Foundation of Shanxi Province (No. 2009011049-3 , 2009011046 , 20051043 ), Specialized Research Fund for the Doctoral Program of Higher Education (SRFDP, No. 20091401110002 ), Program for New Century Excellent Talents in University (No. NCET-10-0927 ), Research Project Supported by Shanxi Scholarship Council of China (No. 2011-013 ), and Program for the Top Young Academic Leaders of Higher Learning Institutions of Shanxi .
PY - 2012/4/30
Y1 - 2012/4/30
N2 - Epidemiological studies suggest that particulate matter (PM 10) inhalation was associated with adverse effects on brain-related health, however, existing experimental data lacked relevant evidences. In this study, we treated Wistar rats with PM 10 at different concentrations (0.3, 1, 3 and 10mg/kg body weight (bw)), and investigated endothelial dysfunction and inflammatory responses in the brain. The results indicate that mild pathological abnormal occurred after 15-day exposure (five times with 3 days each), followed by the changes of endothelial mediators (ET-1 and eNOS) and inflammatory markers (IL-1β, TNF-α, COX-2, iNOS and ICAM-1). Also, the sample up-regulated bax/bcl-2 ratio and p53 expression, and induced neuronal apoptosis. It implicates that PM 10 exerted injuries to mammals' brain, and the mechanisms might be involved in endothelial dysfunction and inflammatory responses.
AB - Epidemiological studies suggest that particulate matter (PM 10) inhalation was associated with adverse effects on brain-related health, however, existing experimental data lacked relevant evidences. In this study, we treated Wistar rats with PM 10 at different concentrations (0.3, 1, 3 and 10mg/kg body weight (bw)), and investigated endothelial dysfunction and inflammatory responses in the brain. The results indicate that mild pathological abnormal occurred after 15-day exposure (five times with 3 days each), followed by the changes of endothelial mediators (ET-1 and eNOS) and inflammatory markers (IL-1β, TNF-α, COX-2, iNOS and ICAM-1). Also, the sample up-regulated bax/bcl-2 ratio and p53 expression, and induced neuronal apoptosis. It implicates that PM 10 exerted injuries to mammals' brain, and the mechanisms might be involved in endothelial dysfunction and inflammatory responses.
KW - Apoptosis
KW - Brain
KW - Endothelial dysfunction
KW - Inflammatory response
KW - PM
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U2 - 10.1016/j.jhazmat.2012.01.034
DO - 10.1016/j.jhazmat.2012.01.034
M3 - Article
C2 - 22365138
AN - SCOPUS:84862820146
SN - 0304-3894
VL - 213-214
SP - 28
EP - 37
JO - Journal of Hazardous Materials
JF - Journal of Hazardous Materials
ER -