PMID- 29269294
OWN - NLM
STAT- MEDLINE
DCOM- 20180213
LR  - 20180213
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 495
IP  - 3
DP  - 2018 Jan 15
TI  - Oxidative stress induced necroptosis activation is involved in the pathogenesis 
      of hyperoxic acute lung injury.
PG  - 2178-2183
LID - S0006-291X(17)32494-4 [pii]
LID - 10.1016/j.bbrc.2017.12.100 [doi]
AB  - Necroptosis has been found to be involved in the pathogenesis of some lung 
      diseases, but its role in hyperoxic acute lung injury (HALI) is still unclear. 
      This study aimed to investigate contribution of necroptosis to the pathogenesis 
      of HALI induced by hyperbaric hyperoxia exposure in a rat model. Rats were 
      divided into control group, HALI group, Nec-1 (necroptosis inhibitor) group and 
      edaravone group. Rats were exposed to pure oxygen at 250 kPa for 6 h to induce 
      HALI. At 30 min before hyperoxia exposure, rats were intraperitoneally injected 
      with Nec-1 or edaravone, and sacrificed at 24 h after hyperoxia exposure. Lung 
      injury was evaluated by histology, lung water to dry ratio (W/D) and 
      bronchoalveolar lavage fluid (BALF) biochemistry; the serum and plasma oxidative 
      stress, expression of RIP1, RIP3 and MLKL, and interaction between RIP1 and RIP3 
      were determined. Results showed hyperoxia exposure significantly caused damage to 
      lung and increased necroptotic cells and the expression of RIP1, RIP3 and MLKL. 
      Edaravone pre-treatment not only inhibited the oxidative stress in HALI, but also 
      reduced necroptotic cells, decreased the expression of RIP1, RIP3 and MLKL and 
      improved lung pathology. Nec-1 pretreatment inhibited necroptosis and improved 
      lung pathology, but had little influence on oxidative stress. This study suggests 
      hyperoxia exposure induces oxidative stress may activate necroptosis, involving 
      in the pathology of HALI, and strategies targeting necroptosis may become 
      promising treatments for HALI.
CI  - Copyright (c) 2017. Published by Elsevier Inc.
FAU - Han, C H
AU  - Han CH
AD  - Department of Pathology, The First Hospital of Jining City, Jining City, Shandong 
      Province, 272011, China.
FAU - Guan, Z B
AU  - Guan ZB
AD  - Department of Respiratory Diseases, The 411th Hospital of People's Liberation 
      Army, Shanghai, 200081, China.
FAU - Zhang, P X
AU  - Zhang PX
AD  - Department of Cardiothoracic Surgery, The First Hospital of Jining City, Jining 
      City, Shandong Province, 272011, China.
FAU - Fang, H L
AU  - Fang HL
AD  - Department of Pathology, The First Hospital of Jining City, Jining City, Shandong 
      Province, 272011, China.
FAU - Li, L
AU  - Li L
AD  - Department of Pathology, The First Hospital of Jining City, Jining City, Shandong 
      Province, 272011, China.
FAU - Zhang, H M
AU  - Zhang HM
AD  - Department of Pathology, The First Hospital of Jining City, Jining City, Shandong 
      Province, 272011, China.
FAU - Zhou, F J
AU  - Zhou FJ
AD  - Department of Pathology, The First Hospital of Jining City, Jining City, Shandong 
      Province, 272011, China.
FAU - Mao, Y F
AU  - Mao YF
AD  - Department of Anesthesiology and Surgical Intensive Care Unit, XinHua Hospital, 
      School of Medicine, Shanghai Jiao Tong University, Shanghai, 200092, China. 
      Electronic address: maoyanfei@xinhuamed.com.cn.
FAU - Liu, W W
AU  - Liu WW
AD  - Department of Diving and Hyperbaric Medicine, The Naval Medical University, 
      Shanghai, 200433, China. Electronic address: wwliu@smmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171218
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Bronchopulmonary Dysplasia/*metabolism/*pathology
MH  - Male
MH  - Necrosis/metabolism/pathology
MH  - *Oxidative Stress
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species/*metabolism
OTO - NOTNLM
OT  - Hyperoxic acute lung injury
OT  - MLKL
OT  - Necroptosis
OT  - RIP1
OT  - RIP3
OT  - Reactive oxygen species
EDAT- 2017/12/23 06:00
MHDA- 2018/02/14 06:00
CRDT- 2017/12/23 06:00
PHST- 2017/12/08 00:00 [received]
PHST- 2017/12/18 00:00 [accepted]
PHST- 2017/12/23 06:00 [pubmed]
PHST- 2018/02/14 06:00 [medline]
PHST- 2017/12/23 06:00 [entrez]
AID - S0006-291X(17)32494-4 [pii]
AID - 10.1016/j.bbrc.2017.12.100 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Jan 15;495(3):2178-2183. doi: 
      10.1016/j.bbrc.2017.12.100. Epub 2017 Dec 18.