PMID- 29793105
OWN - NLM
STAT- MEDLINE
DCOM- 20180926
LR  - 20181004
IS  - 1873-6424 (Electronic)
IS  - 0269-7491 (Linking)
VI  - 241
DP  - 2018 Oct
TI  - COPD rat model is more susceptible to cold stress and PM(2.5) exposure and the 
      underlying mechanism.
PG  - 26-34
LID - S0269-7491(17)34898-4 [pii]
LID - 10.1016/j.envpol.2018.05.034 [doi]
AB  - The purpose of this study is to verify the hypothesis that chronic obstructive 
      pulmonary disease (COPD) model rat is more susceptible to cold stress and fine 
      particulate matter (PM(2.5)) exposure than the healthy rat, and explore the 
      related mechanism. COPD rat model, established with cigarette smoke and 
      lipopolysaccharide intratracheal instillation, were exposed to cold stress (0  degrees C) 
      and PM(2.5) (0, 3.2, 12.8 mg/ml). After that, the levels of superoxide dismutase, 
      inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha), 
      monocyte chemotactic protein 1 (MCP-1) and angiotensin Ⅱ (Ang-Ⅱ) in lung were 
      measured, as well as the expression levels of lung 8-hydroxy-2-deoxyguanosine 
      (8-OHdG), nuclear factor kappa B (NF-kappaB), heme-oxygenase-1 (HO-1) and nuclear 
      factor erythroid-2-related factor 2 (Nrf2). There were significant positive 
      relationships between PM(2.5) and lung level of iNOS, TNF-alpha, MCP-1 and Ang-Ⅱ, 
      lung function and pathologic damage in COPD rats. The HO-1, NF-kappaB and 8-OHdG were 
      found highly expressed in COPD rat lung, particularly at the higher PM(2.5) dose 
      of cold stress groups, while Nrf2 was found declined. Thus, COPD rats may be more 
      susceptible to cold stress and PM(2.5) exposure. Cold stress may aggravate 
      PM(2.5)-induced toxic effects in the lung of COPD rats through increasing 
      Ang-Ⅱ/NF-kappaB signaling pathway and suppressing Nrf2 signaling pathway.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Zhang, Kai
AU  - Zhang K
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Guo, Lei
AU  - Guo L
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Wei, Qiaozhen
AU  - Wei Q
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Song, Quanquan
AU  - Song Q
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Liu, Jiangtao
AU  - Liu J
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Niu, Jingping
AU  - Niu J
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Zhang, Li
AU  - Zhang L
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Ruan, Ye
AU  - Ruan Y
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China.
FAU - Luo, Bin
AU  - Luo B
AD  - Institute of Occupational Health and Environmental Health, School of Public 
      Health, Lanzhou University, Lanzhou, Gansu 730000, People's Republic of China. 
      Electronic address: luob@lzu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20180521
PL  - England
TA  - Environ Pollut
JT  - Environmental pollution (Barking, Essex : 1987)
JID - 8804476
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NF-kappa B)
RN  - 0 (Particulate Matter)
RN  - 0 (Smoke)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
SB  - IM
MH  - Animals
MH  - *Cold Temperature
MH  - Lung/drug effects
MH  - Male
MH  - Models, Biological
MH  - NF-E2-Related Factor 2/metabolism
MH  - NF-kappa B/metabolism
MH  - Nitric Oxide Synthase Type II/metabolism
MH  - Particulate Matter/*toxicity
MH  - Pulmonary Disease, Chronic Obstructive/metabolism/*pathology
MH  - Rats
MH  - Signal Transduction/drug effects
MH  - Smoke
MH  - *Stress, Physiological
MH  - Superoxide Dismutase/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
OTO - NOTNLM
OT  - Ang-Ⅱ
OT  - Chronic obstructive pulmonary disease
OT  - Cold stress
OT  - NF-kappaB
OT  - Nrf2
OT  - PM(2.5)
EDAT- 2018/05/25 06:00
MHDA- 2018/09/27 06:00
CRDT- 2018/05/25 06:00
PHST- 2017/11/24 00:00 [received]
PHST- 2018/05/11 00:00 [revised]
PHST- 2018/05/11 00:00 [accepted]
PHST- 2018/05/25 06:00 [pubmed]
PHST- 2018/09/27 06:00 [medline]
PHST- 2018/05/25 06:00 [entrez]
AID - S0269-7491(17)34898-4 [pii]
AID - 10.1016/j.envpol.2018.05.034 [doi]
PST - ppublish
SO  - Environ Pollut. 2018 Oct;241:26-34. doi: 10.1016/j.envpol.2018.05.034. Epub 2018 
      May 21.